Plant sterol ester of α-linolenic acid ameliorates high-fat diet-induced nonalcoholic fatty liver disease in mice: association with regulating mitochondrial dysfunction and oxidative stress <i>via</i> activating AMPK signaling

Han, Hao; Li, Xiaoyü; Guo, Yan; Zheng, Mingming; Xue, Tingli; Wang, Linqi

doi:10.1039/d0fo02623a

Cited by 27 publications

(20 citation statements)

References 65 publications

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“…Moreover that, mitochondrial dysfunction manifested by mitochondrial swelling and loss of cristae. Similar to our findings, these structural and ultrastructural changes of hepatocytes have been observed in animal models and patients of NAFLD [16], [17].…”

Section: : Photomicrographs Of Immunostained Liver Sections For Caspa...supporting

confidence: 92%

Potential Protective Effect of Zingiber officinale in Comparison to Rosuvastatin on High-fat diet-induced Non-alcoholic Fatty Liver Disease in Rats

Ramadan

Nasr

El-Hay

et al. 2022

Open Access Maced J Med Sci

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BACKGROUND: Non-alcoholic fatty liver disease (NAFLD) is a common liver disease affecting nearly 25% of adults worldwide with related risk factors including obesity, metabolic, and inflammatory diseases. Many therapeutic remedies of natural or synthetic properties were used. AIM: This study aimed to investigate and compare the effects of ginger/rosuvastatin (ROSU) on the liver of rats with induced NAFLD. MATERIALS AND METHODS: Forty adult male albino rats were used in this study and divided into four equal subgroups, Group I, control received the standard rat chow diet and given normal saline (1 ml/kg/day), Group II, high-fat diet (HFD) group, Group III, received HFD+ ROSU (15 mg/kg/day), and Group IV, HFD+ Zingiber officinale (10% W/V) for 6 weeks. At the end of our experiment, the rats were sacrificed then blood samples were collected for biochemical analysis of lipid profiles and liver enzymes, liver specimen was prepared for light and electron microscopic examination, and measurement of tissue level of malondialdehyde. RESULTS: NAFLD caused degenerative changes and lipid deposition in liver cells as evidenced by microscopic results and laboratory tests. Treatment with ginger/ROSU alleviated those changes. CONCLUSION: Ginger and ROSU could ameliorate liver functions in NAFLD and ginger effect is superior to ROSU.

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Section: : Photomicrographs Of Immunostained Liver Sections For Caspa...supporting

confidence: 92%

Potential Protective Effect of Zingiber officinale in Comparison to Rosuvastatin on High-fat diet-induced Non-alcoholic Fatty Liver Disease in Rats

Ramadan

Nasr

El-Hay

et al. 2022

Open Access Maced J Med Sci

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“…A potential clue for the role of ROS in NAFLD progression arises from the therapeutic use of antioxidants. Antioxidants such as sterol ester of alpha‐linolenic acid, 211 physalin B, 212 N‐acetyl cysteine, 213 or vitamin E and vitamin C 214 showed beneficial effects against liver injury, including fibrosis, in the context of NAFLD. Still, a meta‐analysis of randomized trials for treating NAFLD found that those including antioxidants gave mixed results 215 .…”

Section: Ros and Rns Culprits Or Bystanders Of Nafld Progressionmentioning

confidence: 99%

Mitochondria, oxidative stress and nonalcoholic fatty liver disease: A complex relationship

Karkucińska-Więckowska

Simões

Kalinowski

et al. 2021

Eur J Clin Investigation

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According to the ‘multiple‐hit’ hypothesis, several factors can act simultaneously in nonalcoholic fatty liver disease (NAFLD) progression. Increased nitro‐oxidative (nitroso‐oxidative) stress may be considered one of the main contributors involved in the development and risk of NAFLD progression to nonalcoholic steatohepatitis (NASH) characterized by inflammation and fibrosis. Moreover, it has been repeatedly postulated that mitochondrial abnormalities are closely related to the development and progression of liver steatosis and NAFLD pathogenesis. However, it is difficult to determine with certainty whether mitochondrial dysfunction or oxidative stress are primary events or a simple consequence of NAFLD development. On the one hand, increasing lipid accumulation in hepatocytes could cause a wide range of effects from mild to severe mitochondrial damage with a negative impact on cell fate. This can start the cascade of events, including an increase of cellular reactive nitrogen species (RNS) and reactive oxygen species (ROS) production that promotes disease progression from simple steatosis to more severe NAFLD stages. On the other hand, progressing mitochondrial bioenergetic catastrophe and oxidative stress manifestation could be considered accompanying events in the vast spectrum of abnormalities observed during the transition from NAFL to NASH and cirrhosis. This review updates our current understanding of NAFLD pathogenesis and clarifies whether mitochondrial dysfunction and ROS/RNS are culprits or bystanders of NAFLD progression.

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“…This signaling pathway serves an important role in mitochondrial biogenesis ( 26 ). The PGC-1α/NRF1/TFAM signaling pathway has previously been demonstrated to be involved in mitochondrial biogenesis in numerous diseases ( 27 , 28 ). Jiang et al ( 29 ) demonstrated that perampanel could improve mitochondrial biogenesis in neuronal cells via activation of the PGC-1α/NRF1 signaling pathway, which thereby exerts an anti-epileptic effect.…”

Section: Discussionmentioning

confidence: 99%

Salvianolic acid A promotes mitochondrial biogenesis and function via regulating the AMPK/PGC‑1α signaling pathway in HUVECs

Wang

Zhang

et al. 2022

Exp Ther Med

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Mitochondrial dysregulation is an important pathology that leads to endothelial dysfunction, and the occurrence and development of cardiovascular diseases. Salvianolic acid A (SAA) has been demonstrated to be effective in the treatment of vascular complications of type 2 diabetes mellitus. Limited information has been reported on the effects of SAA on mitochondrial function in endothelial cells. In the present study, the effects of SAA on mitochondrial biogenesis and the related underlying mechanisms were investigated in human umbilical vein endothelial cells (HUVECs). Mitotracker red staining and transmission electron microscopy were used to evaluate the effect of SAA on mitochondrial quality. The effect of SAA treatment on mitochondrial DNA/nuclear DNA ratio of HUVECs was detected by real-time quantitative PCR. Western blot was used to determine the protein expression levels of complex III and Complex IV of mitochondrial oxidative phosphorylation subunit, and ATP production was determined by ATP test kit. Real-time quantitative PCR and Western blot were used to determine the effects of SAA on the expression of peroxisome proliferator-activated receptor γ coactivator (PGC-1α) and its target genes nuclear respiratory factor 1 (NRF1) and mitochondrial transcription factor A (TFAM) proteins and genes. Finally, in the presence of 5'AMP-activated protein kinase (AMPK) specific inhibitors, the expression of PGC-1α, NRF1 and TFAM proteins and the phosphorylation levels of AMPK and Acetyl CoA Carboxylase (ACC) were detected by Western blot or real-time quantitative PCR. The results showed that SAA treatment significantly promoted mitochondrial biogenesis and enhanced mitochondrial function of HUVECs. SAA significantly increased the expression levels of PGC-1α and its target genes NRF1 and (TFAM), a key regulator of mitochondrial biogenesis in HUVECs. These enhancements were accompanied by significantly increased phosphorylation of AMPK and ACC, and were significantly inhibited by specific AMPK inhibitors. These results suggest that SAA may promote mitochondrial biogenesis in endothelial cells by activating the AMPK-mediated PGC-1α/TFAM signaling pathway. These data provide new insights into the mechanism of action of SAA in treating diabetic vascular complications.

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Plant sterol ester of α-linolenic acid ameliorates high-fat diet-induced nonalcoholic fatty liver disease in mice: association with regulating mitochondrial dysfunction and oxidative stress via activating AMPK signaling

Abstract: Plant sterol ester of α-linolenic acid prevents nonalcoholic fatty liver disease by improving mitochondrial function, modifying lipid metabolism, and inhibiting oxidative stress via AMPK signaling.

Cited by 27 publications

References 65 publications

Potential Protective Effect of Zingiber officinale in Comparison to Rosuvastatin on High-fat diet-induced Non-alcoholic Fatty Liver Disease in Rats

Potential Protective Effect of Zingiber officinale in Comparison to Rosuvastatin on High-fat diet-induced Non-alcoholic Fatty Liver Disease in Rats

Mitochondria, oxidative stress and nonalcoholic fatty liver disease: A complex relationship

Salvianolic acid A promotes mitochondrial biogenesis and function via regulating the AMPK/PGC‑1α signaling pathway in HUVECs

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