Hepatoprotective Effects of Antrodia cinnamomea: The Modulation of Oxidative Stress Signaling in a Mouse Model of Alcohol‐Induced Acute Liver Injury

Abstract

In the present study, the components of A. cinnamomea (AC) mycelia were systematically analyzed. Subsequently, its hepatoprotective effects and the underlying mechanisms were explored using a mouse model of acute alcohol-induced liver injury. AC contained 25 types of fatty acid, 16 types of amino acid, 3 types of nucleotide, and 8 types of mineral. The hepatoprotective effects were observed after 2 weeks of AC treatment at doses of 75 mg/kg, 225 mg/kg, and 675 mg/kg in the mouse model. These effects were indicated by the changes in the levels of aspartate aminotransferase, alanine aminotransferase, several oxidation-related factors, and inflammatory cytokines in serum and/or liver samples. AC reduced the incidence rate of necrosis, inflammatory infiltration, fatty droplets formation, and cell apoptosis in liver detecting via histological and TUNEL assay. In addition, AC reduced the expression of cleaved caspase-3, -8, and -9 and the levels of phosphor-protein kinase B (Akt) and phosphor-nuclear factor-κB (NF-κB) in the liver samples. Collectively, AC-mediated hepatoprotective effects in a mouse model of acute alcohol-induced liver injury are the result of reduction in oxidative stress. This may be associated with Akt/NF-κB signaling. These results provide valuable evidence to support the use of A. cinnamomea as a functional food and/or medicine.

Schisantherin A alleviated alcohol-induced liver injury by the regulation of alcohol metabolism and NF-kB pathway

“…In agreement with previous observations in alcohol-induced liver injury [ 30 , 40 ], we found that the NF-kB pathway in the liver was activated by alcohol feeding. Activation of NF-kB has been reported to contribute to liver injury through production of pro-inflammatory cytokines [ 15 , 47 ].…”

Anti-inflammatory and hepatoprotective effects of exopolysaccharides isolated from Pleurotus geesteranus on alcohol-induced liver injury

“…Alcoholic liver disease (ALD) has become an important public health issue around the world, with a death rate of 20% 1 – 3 . In addition, the incidence of ALD has increased in China as a consequence of an increased frequency of alcohol consumption 4 .…”

“…In addition, induced expression of cyclooxygenase-2 (COX-2) contributes to the inflammatory response and participates in the aggravation of alcohol-induced liver injury 18 . Moreover, nitric oxide (NO) is involved in a wide range of toxic oxidative reactions 1 , and alcohol consumption induces a significant increase in NO levels, as a result of the elevated synthesis of inducible nitric oxide synthase (iNOS) 2 . Therefore, increases in NO generation may be an early indicator of ethanol-induced liver damage, and inhibiting the release of NO is a potential method for controlling inflammation 19 .…”

Antrodia cinnamomea —An updated minireview of its bioactive components and biological activity

“…A. cinnamomea ameliorated liver injury by reducing necrosis, inflammatory infiltration, and cell apoptosis and downregulated cleaved caspase‐3, ‐8, and ‐9, p‐Akt and p‐NF‐ κ B expression levels in liver samples. This hepatoprotective action of A. cinnamomea was recognized by decreased oxidative stress which was correlated with Akt/NF‐ κ B signaling (Liu et al, ).…”