Abstract
The effect of the baicalin, a bio-active flavonoid extracted from Scutellaria baicalensis Georgi, on the carbon tetrachloride (CCl4) 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 CCl4 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 CCl4. 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 CCl4 but suppressed by the treatment of baicalin in a dose-dependent manner, implying that baicalin can attenuated cell apoptosis induced by CCl4. Overall, these results suggest that baicalin effectively protects hepatocytes from the CCl4 oxidative damage, likely due to the inhibition of free radical generation and cell apoptosis during the liver injury.
Highlights
Liver disease is one of the major global challenges
The effects of baicalin on liver function The effect of baicalin on the liver function was evaluated by measuring the therapeutic serum regimens, hyaluronic acid (HA), Procollagen type III (HPCIII), Aspartate aminotransferase (ALT), and Alanine aminotransferase (AST), on the hepatic fibrosis in CCl4 rat model (Hu et al, 2010; Ozer et al, 2010)
The VG staining results indicated that CCl4 treated liver showed extensive changes in microstructures, including marked enlarged domains of portal inflammation, we evaluate the role of baicalin on liver fibrosis induced by CCl4 in rats
Summary
Liver disease is one of the major global challenges. According to the Office for National Statistics in the United Kingdom, liver disease is the fifth most common cause (Toledano et al, 2019). Free radicals, as found during the oxidative process in cells, can attack unsaturated fatty acids of cell membranes, resulting in cell peroxidation, destructing DNA and protein (Sastre et al, 2007) These processes eventually cause various liver injuries. It was found that the baicalin can inhibit the H2O2-induced liver injury caused by suppression of oxidation in the cell (Yu et al, 2020) It can inhibit the activation of redox sensitive nuclear factor-κB (NF-κB) in kidney from the old rats (Liu et al, 2015a; Yin et al, 2018). It eventually leads to damage of cell membrane (Mccay et al, 1984), following by the release of inflammatory mediators from the activated macrophages They are believed to be the cause of the CCl4induced hepatic injury. The possible molecular mechanism and the effect of inhibition of the oxidative stress and inflammation will be discussed
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