Protective Effect of Hericium erinaceus on Alcohol Induced Hepatotoxicity in Mice

Summary

This research investigated how lion’s mane mushroom (Hericium erinaceus) can protect the liver from alcohol-induced damage. The study found that this medicinal mushroom effectively reduced liver inflammation and damage in mice exposed to alcohol. Impact on everyday life: • Offers a potential natural supplement for people concerned about liver health • May help protect against occasional alcohol consumption’s negative effects • Provides evidence for traditional uses of medicinal mushrooms • Could lead to development of new liver-protective supplements • Suggests dietary approaches for supporting liver health

Background

Alcohol is the most widely abused substance globally and a significant cause of liver injury. Long-term alcohol consumption induces oxidative stress in the liver due to imbalance between prooxidant and antioxidant systems. This persistent oxidative stress can lead to fatty liver, inflammation, fibrosis, cirrhosis, and liver cancer. While progress has been made in understanding alcoholic liver disease pathogenesis, the mechanisms are not fully understood.

Objective

To investigate the protective effects of Hericium erinaceus mushroom extract (HEM) on liver injury induced by acute alcohol administration in mice, specifically examining its impact on liver enzymes, oxidative stress markers, and inflammatory pathways.

Results

HEM administration significantly decreased serum ALT, AST, and MDA levels compared to the ethanol-only group. The treatment reduced ethanol-induced elevation of hepatic TAOS and suppressed NF-κB activation. Histopathological observations showed that HEM treatment notably reduced alcohol-induced liver damage, with fewer cavitations and less fibrosis compared to the ethanol-only group.

Conclusion

Hericium erinaceus mushroom extract (200 mg/kg BW) demonstrated significant hepatoprotective effects against acute alcohol-induced liver damage. The protective mechanism appears to work through inhibition of NF-κB activation and reduction of oxidative stress markers.
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