Protective Effect of Spore Powder of Antrodia camphorata ATCC 200183 on CCl4-Induced Liver Fibrosis in Mice.
Yilin RenHua-Xiang LiLingxi ZhouZhen-Ming LuJinsong ShiYan GengZheng-Hong XuPublished in: Nutrients (2020)
Liver fibrosis is a pathological process with intrahepatic diffused deposition of the excess extracellular matrix, which leads to various chronic liver diseases. Drugs with high efficacy and low toxicity for liver fibrosis are still unavailable. Antrodia camphorata has antioxidant, antivirus, antitumor and anti-inflammation roles, and has been used to treat liver diseases in the population. However, the hepatoprotective effects of A. camphorata spores and the mechanisms behind it have not been investigated. In this study, we evaluate the hepatoprotective effect of spore powder of A. camphorata (SP, 100 mg/kg/day or 200 mg/kg/day) on carbon tetrachloride (CCl4)-induced liver fibrosis in mice. SP groups reduced serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities compared with the CCl4 group. SP also showed a decrease in hydroxyproline (Hyp) content in liver tissues. SP improved cell damage and reduced collagen deposition by H&E, Sirius red and Masson staining. Furthermore, SP down-regulated the mRNA levels of α-SMA and Col 1, and the protein expression of α-smooth muscle actin (α-SMA), collagen I (Col 1), tumor necrosis factor alpha (TNF-α), toll like receptor 4 (TLR4) and nuclear factor-Κb (NF-κB) p65. In summary, SP has an ameliorative effect on hepatic fibrosis, probably by inhibiting the activation of hepatic stellate cells, reducing the synthesis of extracellular matrix.
Keyphrases
- liver fibrosis
- toll like receptor
- nuclear factor
- extracellular matrix
- oxidative stress
- smooth muscle
- inflammatory response
- immune response
- diabetic rats
- rheumatoid arthritis
- signaling pathway
- induced apoptosis
- high glucose
- lps induced
- gene expression
- high fat diet induced
- type diabetes
- cell therapy
- liver injury
- metabolic syndrome
- transcription factor
- endothelial cells
- cell proliferation
- endoplasmic reticulum stress
- bone marrow
- cell cycle arrest
- single molecule