Combating Liver Damage: How Mushroom Extract Could Inhibit Fibrosis

Mushroom extract AHCC could inhibit liver fibrosis by suppressing the activation of hepatic stellate cells, offering potential for new treatments.

Chronic liver damage can result in hepatitis, leading to liver fibrosis. The accumulation of collagen and other fibrous tissue worsens when hepatic stellate cells are activated during hepatitis, often progressing to liver cancer or cirrhosis, which can be life-threatening. With no effective drugs available for cirrhosis, inhibiting the activation of stellate cells is viewed as a potential strategy to control the advancement of liver fibrosis ().

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“It is estimated that one out of every 3-4 people worldwide have steatotic liver disease, when there is an abnormal accumulation of lipids, which is a precursor to fibrosis. So, it is important to prevent the progression of liver fibrosis at an early stage,” explained Dr. Hayato Urushima, an Associate Professor of the Graduate School of Medicine at Osaka Metropolitan University.

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How AHCC Inhibits Hepatic Stellate Cell Activation

His research team investigated how AHCC (Active Hexose Correlated Compound), a standardized extract of cultured Lentinula edodes mycelia, protects the liver and its mechanism.

The team administered AHCC to mice and found that the supplement might inhibit the activation of hepatic stellate cells through two channels.

Via the TLR2 (toll-like receptor protein) channel, AHCC induced cytoglobin that decreased reactive oxygen species, while via the TLR4 channel, the supplement suppressed the expression of collagen in the liver of the mice.

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AHCC's Potential in Liver Fibrosis Treatment

“We aim to conduct clinical trials to confirm the efficacy of AHCC in patients with liver fibrosis to build more reliable scientific evidence,” Dr. Urushima stated. The findings were published in the American Journal of Physiology-Gastrointestinal and Liver Physiology.

Reference:

AHCC inhibited hepatic stellate cells activation by regulation of cytoglobin induction via TLR2-SAPK/JNK pathway and collagen production via TLR4-NF-κβ pathway - (https://journals.physiology.org/doi/full/10.1152/ajpgi.00134.2024)

Source-Eurekalert

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