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Ganoderic Acid A Ameliorates Non-Alcoholic Steatohepatitis (NASH) Induced by High-Fat High-Cholesterol Diet in Mice

Summary

This research investigated how a compound called ganoderic acid A, found in medicinal mushrooms, could help treat fatty liver disease. The study showed that this natural compound can reduce liver fat accumulation, inflammation, and scarring in mice with diet-induced liver disease. This finding is significant for everyday life in several ways: • Offers potential natural treatment option for fatty liver disease, which affects up to 30% of people globally • Demonstrates the medicinal value of traditional mushroom-based remedies • Provides hope for people with NASH who currently have limited treatment options • Shows how dietary supplements might help prevent liver disease progression • Highlights the connection between diet, inflammation, and liver health

Background

Non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH) are increasing in prevalence globally, with NASH being a more aggressive form that can lead to cirrhosis and liver cancer. Currently there are no effective treatments besides lifestyle changes. Ganoderic acids from Ganoderma lucidum mushrooms have shown hepatoprotective effects, but their impact on NASH has not been fully explored.

Objective

To investigate whether ganoderic acid A (GAA) can alleviate NASH in mice fed a high-fat high-cholesterol (HFHC) diet and to determine the underlying molecular mechanisms of its effects.

Results

GAA treatment significantly reduced body weight, improved serum lipid profiles, and decreased liver enzymes ALT and AST in HFHC-fed mice. It also reduced hepatic steatosis, inflammation, and fibrosis as shown by histological analysis. GAA suppressed inflammatory cytokines (IL-1β, TNF-α, IL-6) and reduced oxidative stress markers. The treatment also modulated ER stress-related proteins including GRp78, p-eIF-2α, and p-JNK while increasing protective factors like ERp57.

Conclusion

GAA effectively ameliorates NASH in HFHC-fed mice by reducing hepatic steatosis, inflammation, and fibrosis. The mechanism appears to involve suppression of oxidative stress and modulation of the endoplasmic reticulum stress response. These findings suggest GAA could be a potential therapeutic agent for NASH treatment.
  • Published in:Experimental and Therapeutic Medicine,
  • Study Type:Experimental Animal Study,
  • Source: 10.3892/etm.2022.11237
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