Protection of hepatocyte mitochondrial function by blueberry juice and probiotics <i>via</i> SIRT1 regulation in non-alcoholic fatty liver disease

Ren, Tingting; Zhu, Lili; Shen, Yanyan; Mou, Qiuju; Lin, Tao; Han, Feng

doi:10.1039/c8fo02298d

Cited by 28 publications

(18 citation statements)

References 33 publications

(34 reference statements)

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“…Moreover, Sirt1 knockdown by siRNAs markedly abrogated the inhibitory effect of PSPC on PA-induced apoptosis in L02 cells. Consistent with these studies (12,23,35), our results revealed that PSPC might exhibit inhibitory effects on HFD-induced hepatic apoptosis via restoring Sirt1 level.…”

Section: Discussionsupporting

confidence: 91%

“…In this study, HFD remarkably reduced the protein expression of SirT1 as well as its activity in mouse livers, indicating that HFD-induced hepatic apoptosis may be associated with the down-regulation of Sirt1. It has been widely reported that some naturally occurring polyphenols, such as resveratrol, are Sirt1 activators, which exhibit beneficial effects on a variety of diseases including NAFLD (12,35). Our previous study also demonstrated that troxerutin, a flavonoid, markedly renewed Sirt1 levels to protect mouse liver from HFD-induced steatosis (23).…”

Section: Discussionmentioning

confidence: 86%

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Purple sweet potato color protects against hepatocyte apoptosis through Sirt1 activation in high-fat-diet-treated mice

Su¹,

Zhang²,

Chen³

et al. 2020

Food & Nutrition Research

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Background: Recent evidence indicates that the inhibition of hepatocyte apoptosis is possible to develop a potential therapeutic strategy for nonalcoholic fatty liver disease (NAFLD). Our previous work suggested that purple sweet potato color (PSPC), a class of naturally occurring anthocyanins, effectively improved many features of high-fat diet (HFD)-induced NAFLD. However, whether PSPC ameliorates HFD-induced hepatocyte apoptosis has never been investigated. Objective: Here we investigated the effects of PSPC on HFD-induced hepatic apoptosis and the mechanisms underlying these effects. Design: Mice were divided into four groups: Control group, HFD group, HFD + PSPC group and PSPC group. PSPC was administered by daily oral gavage at doses of 700 mg/kg/day for 20 weeks. EX-527 (a SirT1-selective inhibitor) and Sirt1 siRNA were used to demonstrate the Sirt1 dependence of PSPC-mediated effects on apoptotic and survival signaling pathways in vivo and in vitro. Results: Our results showed that PSPC reduced body weights, hepatic triglyceride contents, histopathological lesions and serum ALT levels in a mouse model of NAFLD induced by HFD. Furthermore, PSPC attenuated HFD-induced hepatocyte apoptosis ratio from 7.27 ± 0.92% to 1.79 ± 0.27% in mouse livers, which is insignificant compared with that of controls. Moreover, PSPC activated Sirt1 by boosting NAD + level in HFD-treated mouse livers. Furthermore, PSPC promoted Sirt1-dependent suppression of P53-mediated apoptotic signaling and activation of Akt survival signaling pathway in HFD-treated mouse livers, which was confirmed by EX527 treatment. Moreover, Sirt1 knockdown abolished these ameliorative effects of PSPC on apoptosis and P53 acetylation and protein expression in PA-treated L02 cells. Ultimately, PSPC reduced Caspase-3 activation and Bax level, and elevated the Bcl-2 level in HFD-treated mouse livers. Conclusion: PSPC protected against HFD-induced hepatic apoptosis by promoting Sirt1-dependent inhibition of p53-apoptotic pathway and facilitation of Akt survival pathway. This study indicates that PSPC is a candidate for nutritional intervention of NAFLD.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 86%

Purple sweet potato color protects against hepatocyte apoptosis through Sirt1 activation in high-fat-diet-treated mice

Su¹,

Zhang²,

Chen³

et al. 2020

Food & Nutrition Research

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“…Administration of mitoquinone mesylate (MitoQ), a mitochondrial-targeted antioxidant with high bioavailability, restores hepatic mitochondrial functions and ameliorates glucose intolerance and hepatic steatosis [61][62][63]. Antioxidant foods including blueberry juice and probiotics significantly reduce NAFLD-induced mitochondrial swelling and hepatic necrosis by restoring the mitochondrial respiratory chain function and suppressing the production of ROS [64]. Pretreatment with methionine alleviates the pathological changes associated with NAFLD by increasing GSH levels [60].…”

Section: Oxidative Stressmentioning

confidence: 99%

Role of mitochondrial quality control in the pathogenesis of nonalcoholic fatty liver disease

Toan

Zhou

2020

Aging

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Nutrient oversupply and mitochondrial dysfunction play central roles in nonalcoholic fatty liver disease (NAFLD). The mitochondria are the major sites of β-oxidation, a catabolic process by which fatty acids are broken down. The mitochondrial quality control (MQC) system includes mitochondrial fission, fusion, mitophagy and mitochondrial redox regulation, and is essential for the maintenance of the functionality and structural integrity of the mitochondria. Excessive and uncontrolled production of reactive oxygen species (ROS) in the mitochondria damages mitochondrial components, including membranes, proteins and mitochondrial DNA (mtDNA), and triggers the mitochondrial pathway of apoptosis. The functionality of some damaged mitochondria can be restored by fusion with normally functioning mitochondria, but when severely damaged, mitochondria are segregated from the remaining functional mitochondrial network through fission and are eventually degraded via mitochondrial autophagy, also called as mitophagy. In this review, we describe the functions and mechanisms of mitochondrial fission, fusion, oxidative stress and mitophagy in the development and progression of NAFLD.

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“…[50][51][52] Several studies have demonstrated that SIRT1 reduces oxidative stress and the activation of SIRT1 by polyphenols would be beneficial in therapeutic intervention of a diversity of chronic diseases including hepatic steatosis. [6,[53][54][55] In this study, we observed that SIRT1 expression was reduced in the HF group. The present study was the first to demonstrate that ASE polyphenols and rosuvastatin significantly increased the SIRT1 expression, contributing to the reduction of oxidative stress in the liver and resolution of hepatic steatosis in obese mice.…”

Section: Discussionmentioning

confidence: 92%

Therapeutic effects of açaí seed extract on hepatic steatosis in high-fat diet-induced obesity in male mice: a comparative effect with rosuvastatin

Tavares

Santos

et al. 2020

Journal of Pharmacy and Pharmacology

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Objectives Obesity is considered a risk factor for the development of non-alcoholic fatty liver disease (NAFLD). The hydroalcoholic extract obtained from the ac ßai seed (ASE), rich in proanthocyanidins, has been shown a potential body weight regulator with antioxidant properties. This study aimed to investigate the therapeutic effect of ASE in obesity-associated NAFLD and compare it with Rosuvastatin. Methods Male C57BL/6 mice received a high-fat diet or standard diet for 12 weeks. The treatments with ASE (300 mg/kg per day) or rosuvastatin (20 mg/ kg per day) began in the eighth week until the 12th week. Key findings Our data show that the treatments with ASE and rosuvastatin reduced body weight and hyperglycaemia, improved lipid profile and attenuated hepatic steatosis in HFD mice. ASE and Rosuvastatin reduced HMGCoA-Reductase and SREBP-1C and increased ABGC8 and pAMPK expressions in the liver. Additionally, ASE, but not Rosuvastatin, reduced NPC1L1 and increased ABCG5 and PPAR-a expressions. ASE and rosuvastatin increased SIRT-1 expression and antioxidant defence, although only ASE was able to decrease the oxidative damage in hepatic tissue. Conclusions The therapeutic effect of ASE was similar to that of rosuvastatin in reducing dyslipidemia and hepatic steatosis but was better in reducing oxidative damage and hyperglycaemia.

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Protection of hepatocyte mitochondrial function by blueberry juice and probiotics via SIRT1 regulation in non-alcoholic fatty liver disease

Abstract: Blueberry juice and probiotics improves mitochondrial dysfunction and oxidative stress induced by nonalcoholic fatty liver disease (NAFLD), by modulating the SIRT1 pathway.

Cited by 28 publications

References 33 publications

Purple sweet potato color protects against hepatocyte apoptosis through Sirt1 activation in high-fat-diet-treated mice

Purple sweet potato color protects against hepatocyte apoptosis through Sirt1 activation in high-fat-diet-treated mice

Role of mitochondrial quality control in the pathogenesis of nonalcoholic fatty liver disease

Therapeutic effects of açaí seed extract on hepatic steatosis in high-fat diet-induced obesity in male mice: a comparative effect with rosuvastatin

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