@Article{biocell.2022.013432,
AUTHOR = {MENGTING LI, YI-ER QIU, KAIFENG ZHENG},
TITLE = {The role of baicalin on carbon tetrachloride induced liver fibrosis},
JOURNAL = {BIOCELL},
VOLUME = {46},
YEAR = {2022},
NUMBER = {4},
PAGES = {1089--1096},
URL = {http://www.techscience.com/biocell/v46n4/45967},
ISSN = {1667-5746},
ABSTRACT = {The effect of the baicalin, a bio-active flavonoid extracted from <i>Scutellaria baicalensis</i> Georgi, on the carbon tetrachloride (CCl<sub>4</sub>) induced liver fibrosis was investigated. To compare the effect of baicalin on the liver fibrosis, five different groups of rats treated by 100, 200, and 400 mg/kg baicalin were studied. Upon CCl<sub>4</sub> treatment, the levels of procollagen type III, aspartate aminotransferase, aminotransferase, hyaluronic acid, and hydroxyproline were significantly increased, whereas the superoxide dismutase and glutathione peroxidase content were decreased. These changes in the biochemical parameters, which are associated with liver function, were significantly attenuated by the baicalin treatment, suggesting that baicalin can suppress the liver fibrosis induced by CCl<sub>4</sub>. Moreover, the histological staining analysis demonstrated that baicalin could effectively inhibit the degree of liver cell injury. The protein expression of AKT/JAK2/ERK in the serum were markedly increased by CCl<sub>4</sub> but suppressed by the treatment of baicalin in a dose-dependent manner, implying that baicalin can attenuated cell apoptosis induced by CCl<sub>4</sub>. Overall, these results suggest that baicalin effectively protects hepatocytes from the CCl<sub>4</sub> oxidative damage, likely due to the inhibition of free radical generation and cell apoptosis during the liver injury.},
DOI = {10.32604/biocell.2022.013432}
}