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Madecassoside ameliorates hepatic steatosis in high-fat diet-fed mice through AMPK/autophagy-mediated suppression of ER stress. | LitMetric

AI Article Synopsis

  • - Hepatic endoplasmic reticulum (ER) stress plays a role in the development of liver fat accumulation (hepatic steatosis) linked to obesity, and madecassoside (MA) has anti-inflammatory effects noted in other contexts.
  • - This study investigates the effects of MA on liver cells and obese mice, revealing that MA treatment reduces fat buildup, cell death, and ER stress in liver cells.
  • - The research indicates that MA's beneficial effects are reliant on the activation of AMPK and the process of autophagy, suggesting MA could be an effective treatment for liver fat accumulation in obesity.

Article Abstract

Hepatic endoplasmic reticulum (ER) stress is a contributing factor in the development of hepatic steatosis in obesity. Madecassoside (MA), a pentacyclic triterpene derived from Centella asiatica, is known for its anti-inflammatory properties in the treatment of skin wounds. However, the impact of MA on hepatic ER stress and lipid metabolism in experimental obesity models has not been investigated. In this study, we examined the effects of MA on primary hepatocytes treated with palmitate and the livers of mice fed a high-fat diet (HFD). Our findings demonstrated that MA treatment reduced lipogenic lipid accumulation, apoptosis, and ER stress in hepatocytes. Additionally, MA treatment increased the phosphorylation of AMP-activated protein kinase (AMPK) and markers of autophagy. Importantly, when AMPK was inhibited by small interfering RNA (siRNA) or autophagy was blocked by 3-methyladenine (3MA), the protective effects of MA against ER stress, lipogenic lipid deposition, and apoptosis in palmitate-treated hepatocytes were abolished. These results suggest that MA mitigates hepatic steatosis in obesity through an AMPK/autophagy-dependent pathway. The present study highlights the potential of MA as a promising therapeutic candidate for hepatic steatosis.

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Source
http://dx.doi.org/10.1016/j.bcp.2023.115815DOI Listing

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