Acai berry inflammation -
Euterpe oleracea Mart. Açai contains high amounts of phenolic compounds, such as polyphenols and anthocyanins, which exhibit a beneficial antioxidant activity In preclinical studies, açai prevented metabolic syndrome 13 , obesity-related adiposity, and hepatic steatosis Additionally, the use of açai in animal models prevented the progression of oxidative stress biomarkers 15 along with exhibiting hypocholesterolaemic 16 and hepatoprotective 17 , 18 effects when administered in conjunction with a hyperlipidaemic diet.
The current study was designed to elucidate the contribution of previously unexplored factors of açai administration in an established murine model of NAFLD induced by a high-fat diet. Our results showed that açai treatment improved liver damage parameters, antioxidant status, and reduced inflammation.
In this model other parameters related with the NAFLD progression was not change such as, fibrosis, stress ER-related genes, and caspase-3 CASP-3 protein levels. The açai pulp showed an excellent antioxidant effect against peroxyl radicals, with substantial total oxygen radical absorbance capacity ORAC of Effects of AAE on cell viability.
AAE inhibits the formation of EROS induced by tert-butyl hydroperoxide TBHP in HepG2 cells and different concentrations of AAE. Significantly different values are marked with different superscript letters.
In this study, histological analyses of the liver were performed to evaluate the extent of inflammation and collagen content. These analyses were represented in a histological panel for each group Fig.
Our results indicated that the high fat HF diet was effective in increasing inflammation, as evidenced by increased levels of TNF-α in the serum and the number of inflammatory cells in the liver Table 1 and Fig.
Conversely, the administration of açai prevented the increase of TNF-α in HFA mice. However, no differences were found regarding the collagen area Fig.
AAE reduces steatosis and inflammation. White arrows indicate the presence of inflammatory infiltrate and black arrows point to macrovesicular steatosis.
b Number of inflammatory cells. c Total collagen area. Assessment of food intake indicated that the administration of the HF diet reduced the amount of food intake in both HF and HFA groups.
In addition, we observed that the composition and caloric density of the HF diet increased animal weight gain and adiposity index. In contrast, the administration of açai alone did not alter these parameters. Groups that were fed the HF diet showed increase in liver weight, liver fat percentage, and ALT and TNF-α levels, with these liver changes all being characteristic of steatosis, whereas treatment with açai effectively inhibited the increase of these parameters Table 1.
No effect was detected either for the HF diet or for the açai treatment regarding AST enzyme levels. Glutathione GSH is considered an important antioxidant defence system in its various reduced and oxidised GSSG forms.
The levels of total GSH in açai A , HF, and HFA groups increased; however, the same pattern was not observed for GSSG. In the groups that received açai, GSSG values remained similar to those of the control group Table 2. The activity of endogenous antioxidant enzymes was also determined.
SOD, CAT, and GPx enzymes showed a reduction in the HF group, whereas the activity of glutathione reductase GR in the HF group was higher than that in the untreated control group.
Treatment with açai prevented the HF-diet-mediated reductions in SOD and CAT activity and increase in GR activity. However, it did not promote changes in GPx levels Table 2.
Levels of thiobarbituric acid-reactive substances TBARS serve used as an indicator of lipid peroxidation. The HF group showed approximately 2. Similarly, in the HF group an increase in the expression of oxidized protein was observed although the administration of açai prevented the augmentation of this marker, such that the HFA group exhibited levels similar to those of the normal diet-fed controls Fig.
AAE improves oxidative stress. We observed that our experimental model was not effective in inducing ER stress, nor did açai alter those parameters. No difference was observed between groups when the protein expression of CASP-3 was considered Fig.
Relative mRNA expression of genes in the liver involved in ER stress pathways and apoptosis in mice. In this study, we examined previously unexplored factors of the protective effects of açai in steatotic mice.
We analysed the beneficial effects of açai in factors involved in the progression of NALFD and evidenced that the administration of açai ameliorate the liver damage parameters, inflammation and antioxidant status. In this experimental model other pathways involved did not alters, like collagen content, ER-related stress genes, and CASP-3 production in the experimental groups.
Açai contains several bioactive secondary metabolites, including potential antioxidants, such as flavonoids, mainly anthocyanins and phenolic acids Numerous studies have described the actions of anthocyanins in the regulation of lipid metabolism and inflammation; however, the doses, in most cases, are impractical for a normal human diet.
Therefore, we conducted this investigation using the format AAE and dosing of açai that was previously employed by Guerra, et al. The ORAC value of AAE was However, the extract of açai used in the present study exhibited considerably higher ORAC value than those found in common phenolic-rich fruits such as strawberry and blackberry, with ORAC values in the ripe stage of The response profile of AAE cytotoxicity was similar to that previously demonstrated by Hogan, et al.
Notably, even evaluating higher concentrations of açai over longer exposure periods, we still found that the CC50 values could be considered acceptable.
In addition, AAE exhibited a substantial inhibitory effect on ROS formation in HepG2 cells. These findings differed from those described by Schauss, et al.
We consider that the findings of the present study are particularly relevant because the HepG2 cell line is used to identify toxic compounds in humans as they afford easy manipulation and provide results reproducible in human primary hepatocytes, owing to the metabolic similarity Together, our findings demonstrated that AAE exhibits a marked antioxidant activity, in addition to not presenting cytotoxicity yet effectively inhibiting the production of ROS in vitro.
To facilitate subsequent in vivo analyses, the açai, as a natural and safe source, was used, and the dose managed was the same as that used by Guerra, et al. Notably, the consumption of açai has also previously been shown to have beneficial effects on insulin resistance in overweight individuals In healthy women, the effects of açai consumption at this dose suggested that it affords protection against atherogenesis and other degenerative diseases related to oxidative stress and dysfunctions in lipid metabolism, improved the antioxidant status by increasing the activity of the enzyme catalase and total antioxidant capacity in polymorphonuclear cells, and decreasing the production of oxygen reactive species 24 , Moreover, this dose improved body composition, dietary, clinical, biochemical, and inflammatory parameters in women with obesity In vivo , our results showed that mice fed the HF diet developed hepatic steatosis and some features related to NAFLD progression.
The spectrum of the disease includes oxidative stress, inflammation, activation of liver stellate cell, collagen formation, and consequent fibrosis 5 , our model showed an intense presence of fat droplets, and, in relation to the other markers of progression, we observed inflammation but no collagen deposition in the liver.
These alterations are in accordance with the changes in liver weight, liver fat percentage, and serum levels of ALT. Additionally, these changes, which can be caused by HF diets, increased the production pattern and secretion of proinflammatory cytokines, such as TNF-α.
Thus, our study complements the findings by Guerra, et al. We further demonstrated that açai was able to attenuate hepatic steatosis, as evidenced by the reduction in lipid content and based on histological analyses.
This effect contributed to preventing the increase of liver weight and serum ALT in AAE treated mice. The açai fruit is known to have hepatoprotective effects in different models and similar results were obtained in other studies 13 , 17 , AAE also showed anti-inflammatory potential as evidenced by reduced serum TNF-α levels and inflammatory cells in the liver.
These results are important to reinforce the anti-inflammatory properties of açai, since it has been well documented that TNF-α serum and hepatic levels are increased in patients with NASH, and it correlates with histological severity of liver damage because there is a strong correlation and direct contribution between necro-inflammatory activity and fibrosis in NAFLD progression The inflammatory process has been associated with lipid peroxidation as described in the pathogenesis of NAFLD and is related to the availability of fatty acids.
In the present study, such alterations were evaluated using oxidative stress biomarkers, which indicated an increase in oxidative stress in the mice fed the HF diet as evidenced by the higher concentration of TBARS and the expression of oxidized proteins. Moreover, some studies have demonstrated enhanced lipid peroxidation in situations of NAFLD 31 , 32 as well as oxidized proteins 32 , with the severity of this oxidative stress being significantly attenuated in the presence of açai.
In the present study, we further demonstrated that there is an important relationship between the biomarker of oxidative stress and a proinflammatory cytokine, and also with the lipid content in the liver, demonstrated by the positive correlation between them. Liver changes may amplify the effects of oxidative stress, where, in the depletion of enzymes of the antioxidant defence system, may occur because of the increase of reactive species in the NAFLD 33 , thereby compromising the non-enzymatic and enzymatic antioxidant defences In our study, changes in antioxidant defences were confirmed by the lower activity of GPx, SOD, and CAT enzymes.
The addition of açai resulted in an improvement of the redox balance, consequent to the improvement of the biomarkers of oxidative stress, in addition to reversing the changes of the enzymes CAT and SOD.
However, it is important to note that the presence of phytochemical compounds, especially polyphenols, has been associated with the effects of açai as an antioxidant via both direct 19 and indirect effects 15 , 27 , 34 in different experimental models.
In the same context, the changes of GSH levels mediated by açai in the A and HFA groups might be explained by increased transcription of γ-glutamyl cysteine synthetase, a limiting enzyme in the synthesis of GSH, as demonstrated in previous studies 34 , These results reinforce the antioxidant role of açai and support that the reduction in oxidative stress is important in the protective effect of the fruit in NAFLD.
In accordance with this, Qu, et al. A steatotic liver is more susceptible to circulating fatty acids and their accumulation can induce ER stress and ROS formation, promoting hepatic injury and, in some cases, apoptosis Thus, the restoration of homeostasis in ER may constitute a possible mechanism that could explain the hepatoprotective effects of açai.
To assess whether changes occurred in ER homeostasis in our HF-diet model, we evaluated three molecular markers of the unfolded protein response.
Notably, mRNA expression levels of ATF4 and sXBP1 were low in all groups as compared to those in the control; moreover, the presence of açai did not alter these markers.
Consequently, apoptosis pathways did not appear to be activated, suggested by the equivalent quantification of the CASP-3 protein among groups.
bw for 18 weeks yielded a significant reduction in body weight gain, serum levels of triacylglycerols, total cholesterol, and LDL-cholesterol, as well as liver triacylglycerols and total cholesterol, together with a reduction of the accumulation of intracellular lipid droplets However, the therapeutic potential of açai was similar to that of resveratrol in improving steatosis-related parameters, even at a lower dose and shorter treatment time.
Our data showed a remarkable antioxidant activity in vitro of AAE and efficacy in inhibiting ROS production in HepG2 cells with no cytotoxicity. The intake of açai in physiological doses led to an improved response to oxidative stress and modulates proinflammatory related markers, which are associated with a protective role against NAFLD features in vivo.
These findings indicate the beneficial effects of açai against liver damage with a better understanding of the underlying mechanisms and also provide further evidence of its potential as a nutritional therapy.
A single lot of pasteurized frozen açai pulp without colorants or preservatives was obtained from Icefruit Comércio de Alimentos Ltda. The pulp was thawed, filtered Whatman n°.
Açai pulp proximate composition and phytochemicals content were previously described AAE antioxidant capacity was determined using the ORAC method, adapted from other published methodologies 40 , 41 , The ORAC values were calculated using the regression equation between the concentration of Trolox and the net area under the curve and are expressed as equivalents of μM of Trolox per litre.
AAE cytotoxicity was evaluated by the 3- 4,5-dimethylthiazolyl -2,5-diphenyltetrazolium bromide MTT assay Louis, MO, USA , and fungizone 2. The culture medium was subsequently withdrawn, sterile AAE diluted in DMEM-HG medium at different concentrations 0, Male Swiss mice kindly supplied by the Bioterium of Experimental Nutrition Laboratory, School of Nutrition, Federal University of Ouro Preto UFOP , MG, Brazil, were used and the procedures were carried out in accordance with the approved guidelines and by the Ethics Committee in Animal Research of UFOP Protocol N°.
The control group C received a standard AINM diet Diet composition is described in Table 3. After six weeks, the groups were subdivided into groups C and A standard diet , and HF and HFA HF diet.
Additionally, liver, epididymal, mesenteric, and retroperitoneal white adipose tissue was collected, then washed in saline, dried, and weighed. The adiposity index was determined by the sum of the weights of white adipose tissues divided by bodyweight × and expressed as adiposity percent Serum concentrations of active ALT Cat.
N° 53 , and aspartate aminotransferase AST Cat. N° 52 were determined enzymatically using commercial kits Labtest, Lagoa Santa, Brazil. Serum TNF-α levels were quantified using commercial enzyme-linked immunosorbent assays Mouse TNFα ELISA Kit RABKT; Millipore, Billerica, MA, USA.
SOD was assayed using an SOD kit ; Cayman Chemical Company, Ann Arbor, MI, USA , according to manufacturer instruction. CAT activity was determined as described by Aebi Total GSH content was determined using a kinetic assay by Griffith GPx activity was determined according to a method by Paglia and Valentine 50 with minor modifications.
GR enzymatic activity was determined according to a method by CARLBERG and MANNERVIK The total lipid content in the liver was quantified gravimetrically by solvent evaporation.
Lipid peroxidation was assessed using the TBARS assay by Buege and Aust Total protein concentration in the samples was determined according to Lowry, et al.
Fibrosis and inflammation quantification were assessed by evaluation of the total tissue area 1. Total RNA was isolated from liver using the RNAgents Total RNA Isolation System Z; Promega, Madison, WI, USA according to manufacturer instruction.
qPCR was performed using the Power SYBR® Green PCR Master Mix reagent ; Applied Biosystems according to manufacturer recommendation, using the Applied Biosystems® Real-Time PCR System. Primers are listed in the Supplementary Methods. Total protein concentration was determined using the assay by Lowry, et al.
CASP-3 levels were measured using western blotting and an anti-CASP3 antibody , Caspase-3 8G10 Rabbit mAb , Cell Signaling Technology and anti-rabbit IgG coupled to horseradish peroxidase , anti-rabbit IgG-HRP: sc; Santa Cruz Biotechnology, Dallas, TX, USA.
To detect β-actin, a primary mouse monoclonal anti-β-Actin antibody , A; Sigma-Aldrich and anti-mouse IgG , A; Sigma-Aldrich were used. The first gel was stained with Coomassie Brilliant Blue R , Sigma ; the second was transferred electrophoretically to a nitrocellulose membrane, and processed for western blotting using a rabbit anti-2,4-dinitrophenol antibody , D; Sigma that had been incubated with anti-rabbit IgG-HRP ECL detection and densitometry were performed as described above.
Additional materials and methods are available as supplementary materials at the Science website. Data normality was tested using the Kolmogorov—Smirnov test. Non-parametric data were analysed using the Kruskal—Wallis test and Dunn post hoc test.
The results are expressed as medians and interquartile ranges. All analyses were conducted using GraphPad prism version 5. The experimental data used to support the findings of this study are included in the article and readers can access it through the article content. Raw data regarding the findings and any other information can be requested from the corresponding author of the paper via e-mail.
Nonalcoholic steatohepatitis: summary of an AASLD Single Topic Conference. Hepatology 37 , — Article Google Scholar. Pagliassotti, M. Endoplasmic reticulum stress in nonalcoholic fatty liver disease. Annual review of nutrition 32 , 17—33 Article CAS Google Scholar. Postic, C. The role of the lipogenic pathway in the development of hepatic steatosis.
Dalle-Donne, I. Protein carbonyl groups as biomarkers of oxidative stress. Clinica chimica acta , 23—38 Browning, J. Molecular mediators of hepatic steatosis and liver injury. The Journal of clinical investigation , — Barbosa, K. Pulp from acai berries is sold in the United States in a variety of food products, including smoothies, juices, and even wine.
You may have also seen acai extracts used to make products such as protein powders, vitamin chews, and topical ointments. Little is known about the safety of acai supplements. Both acai berries and blueberries contain antioxidants called proanthocyanidins and are considered healthy functional foods.
Additionally, acai berries offer healthy fats. You should also refrain from drinking unprocessed acai juice because it carries a risk of parasitic infection.
In terms of antioxidants , acai berries contain a group of antioxidants called proanthocyanidins, which are similar to those in blueberries, according to the University of Wisconsin in Madison. They also contain oleic acid, a type of monounsaturated fatty acid.
Per the U. Department of Agriculture USDA , a gram g or ¼ cup serving of acai berry puree contains:. Like other berries such as blackberries, blueberries, and raspberries, acai berries are naturally rich in antioxidants.
Research shows these plant-based compounds may help reduce cellular damage in the body that could eventually lead to chronic illnesses. The densest source of these antioxidants are anthocyanins, which are the same compounds that give acai berries their rich color, explains Best.
According to the NCCIH, antioxidants in acai berries may have these effects in humans. This could translate to numerous health benefits, including the following.
Antioxidants help prevent cellular damage from free radicals, which can subsequently lead to cancer. According to Daily, the antioxidant profile of acai berries goes beyond anthocyanins. Additionally, research in rodents suggests that acai may be useful as a complementary cancer treatment to reduce the growth of tumors.
Human studies are needed to confirm such effects. Studies have looked at the potential of antioxidant-rich foods like acai berries to play a role in fighting the inflammation that underlies cardiovascular diseases. One comparative study , for example, found that acai did as much to reverse high blood pressure and cardiac changes in rats with renovascular hypertension as an ACE inhibitor called enalapril.
The components of acai may also have brain-health benefits. The anti-inflammatory effects of acai may also help with nonalcoholic fatty liver disease, as suggested by research that found acai improved blood lipids and overall liver health in rodents after 10 weeks.
That said, additional studies on human are needed to determine whether acai may directly treat any liver disease. No human studies have shown that acai berries offer any effects on weight loss. Both Best and Nicolai caution against using any one food as a weight loss agent.
As Britannica explains, this is because acai berries are highly perishable. Instead, farmers process acai berries for their pulp, which is then used in a variety of food products and supplements. You can find acai berries in juices, smoothies, and fruit bowls. They may also be available in supplements, such as tablets, chewables, and powders.
Both acai food products and supplements may be available in grocery stores, supermarkets, or health food stores. Nicolai encourages shoppers to read ingredient labels carefully.
Acai food products are available in either the refrigerated or freezer sections of the grocery store — read the individual product labels carefully for expiration dates. Acai-based supplements, on the other hand, require storage in a cool, dry location, such as a pantry or medicine cabinet.
Additionally, acai berries may be available in supplemental form. The NCCIH also says that acai berry foods are generally considered safe. But there may be risks associated with drinking unprocessed acai juice, as well as supplements.
Most acai berry foods, such as the pulp and puree form, may be safe to consume in your diet. But there are some side effects and precautions to consider:. Blood samples taken before juice consumption, and again after consumption, showed significant increases in blood antioxidant levels after two hours.
The researchers also noted a significant inhibition of lipid peroxidation - a marker of oxidative stress - in the volunteers. The researchers stated that the antioxidant profile of the juice as key to the apparent benefits. In addition to açai, the juice also contained white and purple grape, Nashi pear, acerola, aronia, cranberry, passion fruit, apricot, prune, kiwifruit, blueberry, wolfberry, pomegranate, lychee, camu camu, pear, banana, and bilberry.
If the study can be repeated in other human studies with larger numbers of participants, the juice could offers promise for preventing chronic inflammation, brought about by an over-expression or lack of control of the normal protective mechanism.
Chronic inflammation has been linked to range of conditions linked to heart disease, osteoporosis, cognitive decline and Alzheimer's, type-2 diabetes, and arthritis. Jensen, X. Wu, K. Patterson, J. Barnes, S. Carter, L. Scherwitz, R.
In the last several years, you Inflammaton have noticed the prevalence Quercetin benefits acai berries and acai innflammation products in grocery chains and health niflammation stores. Acai berryy come Acai berry inflammation Hypertension risk reduction techniques palm tree of the same name. Indigenous to both Central and South America, the deep purple berries are a key food source for native populations in the Amazon region, according to Britannica. Acai berries also spoil quickly, usually within a day after they're picked. The pulp is frozen to make beverages or dried and ground into a powder.
Acai berry inflammation -
Acai berries are rich in vitamins A and C that are known as promoters of collagen production. Collagen is one of the major building blocks of bones, skin, muscle, tendons, and ligaments. One of the biggest enemies of your skin are environmental aggressors that accelerate skin aging.
Luckily, acai berries are rich in fatty acids that protect the skin from pollutants and other harsh environmental conditions. Since acai berries are a superfood, we will give you some super recipes ideas.
So, you can consume acai berries as juice, in tablet form, dries, frozen, or as powder. When it comes to skincare, acai berry is the best when it is incorporated into a skincare product.
Acai berry activated mask is like that. Pair with UFO or UFO mini to help reveal younger-looking skin in minutes. Get your Acai Berry face mask. The acai berry is one of my favourite masks! I am unsure if the new sheet masks can be used with the ufo?
Hi Tameka darling, sure it can be used with the UFO. Pair the mask with UFO for just 2 minutes and enjoy a soothing facial treatment that will leave your skin plump.
The vibrant colors, the refreshing taste, and the health benefits of this trendy treat have piqued my curiosity and left me longing for the opportunity to savor an acai bowl.
You amplified that by saying that acai berries may enhance brain function by sharpening the intellect and enhancing memory, according to research. Sign me up for the newsletter! Want more MYSA? Sign up for our newsletter! Search for:. Toggle Navigation TOP 10 ARTICLES FOREO News News Products Anti-Aging Products Blackheads and Acne Products Toothbrush Under eyes Products SKINCARE ORAL CARE WELL-BEING NUTRITION FITNESS LIFESTYLE SLEEP BETTER SEXUAL WELLNESS BEAUTY MAKEUP FASHION HAIR.
Contents What is acai berry? Effects of AAE on cell viability. AAE inhibits the formation of EROS induced by tert-butyl hydroperoxide TBHP in HepG2 cells and different concentrations of AAE.
Significantly different values are marked with different superscript letters. In this study, histological analyses of the liver were performed to evaluate the extent of inflammation and collagen content. These analyses were represented in a histological panel for each group Fig.
Our results indicated that the high fat HF diet was effective in increasing inflammation, as evidenced by increased levels of TNF-α in the serum and the number of inflammatory cells in the liver Table 1 and Fig.
Conversely, the administration of açai prevented the increase of TNF-α in HFA mice. However, no differences were found regarding the collagen area Fig.
AAE reduces steatosis and inflammation. White arrows indicate the presence of inflammatory infiltrate and black arrows point to macrovesicular steatosis. b Number of inflammatory cells. c Total collagen area. Assessment of food intake indicated that the administration of the HF diet reduced the amount of food intake in both HF and HFA groups.
In addition, we observed that the composition and caloric density of the HF diet increased animal weight gain and adiposity index. In contrast, the administration of açai alone did not alter these parameters. Groups that were fed the HF diet showed increase in liver weight, liver fat percentage, and ALT and TNF-α levels, with these liver changes all being characteristic of steatosis, whereas treatment with açai effectively inhibited the increase of these parameters Table 1.
No effect was detected either for the HF diet or for the açai treatment regarding AST enzyme levels. Glutathione GSH is considered an important antioxidant defence system in its various reduced and oxidised GSSG forms.
The levels of total GSH in açai A , HF, and HFA groups increased; however, the same pattern was not observed for GSSG. In the groups that received açai, GSSG values remained similar to those of the control group Table 2.
The activity of endogenous antioxidant enzymes was also determined. SOD, CAT, and GPx enzymes showed a reduction in the HF group, whereas the activity of glutathione reductase GR in the HF group was higher than that in the untreated control group.
Treatment with açai prevented the HF-diet-mediated reductions in SOD and CAT activity and increase in GR activity.
However, it did not promote changes in GPx levels Table 2. Levels of thiobarbituric acid-reactive substances TBARS serve used as an indicator of lipid peroxidation.
The HF group showed approximately 2. Similarly, in the HF group an increase in the expression of oxidized protein was observed although the administration of açai prevented the augmentation of this marker, such that the HFA group exhibited levels similar to those of the normal diet-fed controls Fig.
AAE improves oxidative stress. We observed that our experimental model was not effective in inducing ER stress, nor did açai alter those parameters. No difference was observed between groups when the protein expression of CASP-3 was considered Fig.
Relative mRNA expression of genes in the liver involved in ER stress pathways and apoptosis in mice. In this study, we examined previously unexplored factors of the protective effects of açai in steatotic mice. We analysed the beneficial effects of açai in factors involved in the progression of NALFD and evidenced that the administration of açai ameliorate the liver damage parameters, inflammation and antioxidant status.
In this experimental model other pathways involved did not alters, like collagen content, ER-related stress genes, and CASP-3 production in the experimental groups. Açai contains several bioactive secondary metabolites, including potential antioxidants, such as flavonoids, mainly anthocyanins and phenolic acids Numerous studies have described the actions of anthocyanins in the regulation of lipid metabolism and inflammation; however, the doses, in most cases, are impractical for a normal human diet.
Therefore, we conducted this investigation using the format AAE and dosing of açai that was previously employed by Guerra, et al. The ORAC value of AAE was However, the extract of açai used in the present study exhibited considerably higher ORAC value than those found in common phenolic-rich fruits such as strawberry and blackberry, with ORAC values in the ripe stage of The response profile of AAE cytotoxicity was similar to that previously demonstrated by Hogan, et al.
Notably, even evaluating higher concentrations of açai over longer exposure periods, we still found that the CC50 values could be considered acceptable. In addition, AAE exhibited a substantial inhibitory effect on ROS formation in HepG2 cells.
These findings differed from those described by Schauss, et al. We consider that the findings of the present study are particularly relevant because the HepG2 cell line is used to identify toxic compounds in humans as they afford easy manipulation and provide results reproducible in human primary hepatocytes, owing to the metabolic similarity Together, our findings demonstrated that AAE exhibits a marked antioxidant activity, in addition to not presenting cytotoxicity yet effectively inhibiting the production of ROS in vitro.
To facilitate subsequent in vivo analyses, the açai, as a natural and safe source, was used, and the dose managed was the same as that used by Guerra, et al.
Notably, the consumption of açai has also previously been shown to have beneficial effects on insulin resistance in overweight individuals In healthy women, the effects of açai consumption at this dose suggested that it affords protection against atherogenesis and other degenerative diseases related to oxidative stress and dysfunctions in lipid metabolism, improved the antioxidant status by increasing the activity of the enzyme catalase and total antioxidant capacity in polymorphonuclear cells, and decreasing the production of oxygen reactive species 24 , Moreover, this dose improved body composition, dietary, clinical, biochemical, and inflammatory parameters in women with obesity In vivo , our results showed that mice fed the HF diet developed hepatic steatosis and some features related to NAFLD progression.
The spectrum of the disease includes oxidative stress, inflammation, activation of liver stellate cell, collagen formation, and consequent fibrosis 5 , our model showed an intense presence of fat droplets, and, in relation to the other markers of progression, we observed inflammation but no collagen deposition in the liver.
These alterations are in accordance with the changes in liver weight, liver fat percentage, and serum levels of ALT. Additionally, these changes, which can be caused by HF diets, increased the production pattern and secretion of proinflammatory cytokines, such as TNF-α. Thus, our study complements the findings by Guerra, et al.
We further demonstrated that açai was able to attenuate hepatic steatosis, as evidenced by the reduction in lipid content and based on histological analyses. This effect contributed to preventing the increase of liver weight and serum ALT in AAE treated mice. The açai fruit is known to have hepatoprotective effects in different models and similar results were obtained in other studies 13 , 17 , AAE also showed anti-inflammatory potential as evidenced by reduced serum TNF-α levels and inflammatory cells in the liver.
These results are important to reinforce the anti-inflammatory properties of açai, since it has been well documented that TNF-α serum and hepatic levels are increased in patients with NASH, and it correlates with histological severity of liver damage because there is a strong correlation and direct contribution between necro-inflammatory activity and fibrosis in NAFLD progression The inflammatory process has been associated with lipid peroxidation as described in the pathogenesis of NAFLD and is related to the availability of fatty acids.
In the present study, such alterations were evaluated using oxidative stress biomarkers, which indicated an increase in oxidative stress in the mice fed the HF diet as evidenced by the higher concentration of TBARS and the expression of oxidized proteins.
Moreover, some studies have demonstrated enhanced lipid peroxidation in situations of NAFLD 31 , 32 as well as oxidized proteins 32 , with the severity of this oxidative stress being significantly attenuated in the presence of açai.
In the present study, we further demonstrated that there is an important relationship between the biomarker of oxidative stress and a proinflammatory cytokine, and also with the lipid content in the liver, demonstrated by the positive correlation between them. Liver changes may amplify the effects of oxidative stress, where, in the depletion of enzymes of the antioxidant defence system, may occur because of the increase of reactive species in the NAFLD 33 , thereby compromising the non-enzymatic and enzymatic antioxidant defences In our study, changes in antioxidant defences were confirmed by the lower activity of GPx, SOD, and CAT enzymes.
The addition of açai resulted in an improvement of the redox balance, consequent to the improvement of the biomarkers of oxidative stress, in addition to reversing the changes of the enzymes CAT and SOD.
However, it is important to note that the presence of phytochemical compounds, especially polyphenols, has been associated with the effects of açai as an antioxidant via both direct 19 and indirect effects 15 , 27 , 34 in different experimental models.
In the same context, the changes of GSH levels mediated by açai in the A and HFA groups might be explained by increased transcription of γ-glutamyl cysteine synthetase, a limiting enzyme in the synthesis of GSH, as demonstrated in previous studies 34 , These results reinforce the antioxidant role of açai and support that the reduction in oxidative stress is important in the protective effect of the fruit in NAFLD.
In accordance with this, Qu, et al. A steatotic liver is more susceptible to circulating fatty acids and their accumulation can induce ER stress and ROS formation, promoting hepatic injury and, in some cases, apoptosis Thus, the restoration of homeostasis in ER may constitute a possible mechanism that could explain the hepatoprotective effects of açai.
To assess whether changes occurred in ER homeostasis in our HF-diet model, we evaluated three molecular markers of the unfolded protein response. Notably, mRNA expression levels of ATF4 and sXBP1 were low in all groups as compared to those in the control; moreover, the presence of açai did not alter these markers.
Consequently, apoptosis pathways did not appear to be activated, suggested by the equivalent quantification of the CASP-3 protein among groups. bw for 18 weeks yielded a significant reduction in body weight gain, serum levels of triacylglycerols, total cholesterol, and LDL-cholesterol, as well as liver triacylglycerols and total cholesterol, together with a reduction of the accumulation of intracellular lipid droplets However, the therapeutic potential of açai was similar to that of resveratrol in improving steatosis-related parameters, even at a lower dose and shorter treatment time.
Our data showed a remarkable antioxidant activity in vitro of AAE and efficacy in inhibiting ROS production in HepG2 cells with no cytotoxicity. The intake of açai in physiological doses led to an improved response to oxidative stress and modulates proinflammatory related markers, which are associated with a protective role against NAFLD features in vivo.
These findings indicate the beneficial effects of açai against liver damage with a better understanding of the underlying mechanisms and also provide further evidence of its potential as a nutritional therapy. A single lot of pasteurized frozen açai pulp without colorants or preservatives was obtained from Icefruit Comércio de Alimentos Ltda.
The pulp was thawed, filtered Whatman n°. Açai pulp proximate composition and phytochemicals content were previously described AAE antioxidant capacity was determined using the ORAC method, adapted from other published methodologies 40 , 41 , The ORAC values were calculated using the regression equation between the concentration of Trolox and the net area under the curve and are expressed as equivalents of μM of Trolox per litre.
AAE cytotoxicity was evaluated by the 3- 4,5-dimethylthiazolyl -2,5-diphenyltetrazolium bromide MTT assay Louis, MO, USA , and fungizone 2. The culture medium was subsequently withdrawn, sterile AAE diluted in DMEM-HG medium at different concentrations 0, Male Swiss mice kindly supplied by the Bioterium of Experimental Nutrition Laboratory, School of Nutrition, Federal University of Ouro Preto UFOP , MG, Brazil, were used and the procedures were carried out in accordance with the approved guidelines and by the Ethics Committee in Animal Research of UFOP Protocol N°.
The control group C received a standard AINM diet Diet composition is described in Table 3. After six weeks, the groups were subdivided into groups C and A standard diet , and HF and HFA HF diet. Additionally, liver, epididymal, mesenteric, and retroperitoneal white adipose tissue was collected, then washed in saline, dried, and weighed.
The adiposity index was determined by the sum of the weights of white adipose tissues divided by bodyweight × and expressed as adiposity percent Serum concentrations of active ALT Cat.
N° 53 , and aspartate aminotransferase AST Cat. N° 52 were determined enzymatically using commercial kits Labtest, Lagoa Santa, Brazil. Serum TNF-α levels were quantified using commercial enzyme-linked immunosorbent assays Mouse TNFα ELISA Kit RABKT; Millipore, Billerica, MA, USA.
SOD was assayed using an SOD kit ; Cayman Chemical Company, Ann Arbor, MI, USA , according to manufacturer instruction. CAT activity was determined as described by Aebi Total GSH content was determined using a kinetic assay by Griffith GPx activity was determined according to a method by Paglia and Valentine 50 with minor modifications.
GR enzymatic activity was determined according to a method by CARLBERG and MANNERVIK The total lipid content in the liver was quantified gravimetrically by solvent evaporation.
Lipid peroxidation was assessed using the TBARS assay by Buege and Aust Total protein concentration in the samples was determined according to Lowry, et al. Fibrosis and inflammation quantification were assessed by evaluation of the total tissue area 1.
Total RNA was isolated from liver using the RNAgents Total RNA Isolation System Z; Promega, Madison, WI, USA according to manufacturer instruction. qPCR was performed using the Power SYBR® Green PCR Master Mix reagent ; Applied Biosystems according to manufacturer recommendation, using the Applied Biosystems® Real-Time PCR System.
Primers are listed in the Supplementary Methods. Total protein concentration was determined using the assay by Lowry, et al. CASP-3 levels were measured using western blotting and an anti-CASP3 antibody , Caspase-3 8G10 Rabbit mAb , Cell Signaling Technology and anti-rabbit IgG coupled to horseradish peroxidase , anti-rabbit IgG-HRP: sc; Santa Cruz Biotechnology, Dallas, TX, USA.
To detect β-actin, a primary mouse monoclonal anti-β-Actin antibody , A; Sigma-Aldrich and anti-mouse IgG , A; Sigma-Aldrich were used. The first gel was stained with Coomassie Brilliant Blue R , Sigma ; the second was transferred electrophoretically to a nitrocellulose membrane, and processed for western blotting using a rabbit anti-2,4-dinitrophenol antibody , D; Sigma that had been incubated with anti-rabbit IgG-HRP ECL detection and densitometry were performed as described above.
Additional materials and methods are available as supplementary materials at the Science website. Data normality was tested using the Kolmogorov—Smirnov test. Non-parametric data were analysed using the Kruskal—Wallis test and Dunn post hoc test. The results are expressed as medians and interquartile ranges.
All analyses were conducted using GraphPad prism version 5. The experimental data used to support the findings of this study are included in the article and readers can access it through the article content.
Raw data regarding the findings and any other information can be requested from the corresponding author of the paper via e-mail.
Nonalcoholic steatohepatitis: summary of an AASLD Single Topic Conference. Hepatology 37 , — Article Google Scholar. Pagliassotti, M. Endoplasmic reticulum stress in nonalcoholic fatty liver disease. Annual review of nutrition 32 , 17—33 Article CAS Google Scholar. Postic, C.
The role of the lipogenic pathway in the development of hepatic steatosis. Dalle-Donne, I. Protein carbonyl groups as biomarkers of oxidative stress. Clinica chimica acta , 23—38 Browning, J. Molecular mediators of hepatic steatosis and liver injury.
The Journal of clinical investigation , — Barbosa, K. et al. Oxidative stress: concept, implications and modulating factors. Revista de Nutrição 23 , — Malhi, H. Endoplasmic reticulum stress in liver disease.
Journal of hepatology 54 , — Tabas, I. Integrating the mechanisms of apoptosis induced by endoplasmic reticulum stress. If the study can be repeated in other human studies with larger numbers of participants, the juice could offers promise for preventing chronic inflammation, brought about by an over-expression or lack of control of the normal protective mechanism.
Chronic inflammation has been linked to range of conditions linked to heart disease, osteoporosis, cognitive decline and Alzheimer's, type-2 diabetes, and arthritis.
Jensen, X. Wu, K. Patterson, J. Barnes, S. Carter, L. Scherwitz, R. Beaman, J. Endres, A. Show more. Content provided by Natural Remedies Private Limited Jan White Paper.
Açai berries Infoammation ah-sigh-ee Quercetin benefits inflammatioon formed inflammxtion of the Respiratory health awareness diet of Inflanmation tribes. Inflaammation the appearance of a purple Quercetin benefits and taste of a tropical berry, it inflammahion been shown Lentils variety pack have powerful Quercetin benefits properties inflammmation to a high level Acai berry inflammation anthocyanins, pigments that are also present in red wine. It is presently being sold in a number of countries, including New Zealand, Australia, South America, Japan, USA, and the Middle East. The juice was found to possess a dose-dependent antioxidant activity, and protected cells were protected against oxidative damage. Comparing ORAC antioxidant activity values, the researchers report an ORAC value of The main antioxidants in the juice were primarily anthocyanins, they added, and predominantly cyanidin 3-rutoside, cyanidin 3-diglycoside, and cyanidin 3-glucoside. Jensen and co-workers then recruited 12 healthy subjects average age
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