Baicalein reduces the occurrence of cirrhotic endotoxemia by reducing intestinal mucosal apoptosis

Yi Liu, Feng Ye, Wen-jing Zou, Ye Sun, Rui Wang, Ping-ping Han, Zhe Zhang, Xue-liang Yang, Xiaojin Liu

The dried roots of Scutellaria baicalensis Georgi, is known in traditional Chinese medicine as Huang Qin (H. qin), and it has been officially and traditionally used in treatment of various diseases such as hepatitis in China. Baicalein (BA), a flavonoid originally isolated from H. qin, has shown a wide range of biological activities. This study was to evaluate whether baicalein, can reduce the intestinal mucosal cell apoptosis caused by cirrhotic endotoxemia and its possible mechanisms. For this purpose, compound factors modeling was used to establish endotoxemic cirrhotic rat model. Firstly, we evaluated endotoxin, ALT, AST and TBIL levels after the baicalein treatment (20 mg/kg, i.v.). To investigate the mechanism of baicalein effect on apoptosis, TUNEL assay was used to detect intestinal mucosal apoptosis. RT-PCR was used to detect the expression levels of gene Bcl-2 mRNA and Bax mRNA in intestinal mucosal tissues. Caspase-3 activity of intestinal tissue was detected with colorimetric method in our experiments. After treatment with BA, the serum endotoxin concentration, the intestinal mucosal apoptosis rate and the activity of caspase-3 of the baicalein group were significantly lower than that of the model and the glutamine group. The serum ALT, AST and TBIL concentration of the BA group were significantly lower than that of the model group. The body weight of the baicalein group was significantly lower than that of the normal group, but it was higher than that of the model group. Among the treatment groups, the mRNA level of anti-apoptotic gene Bcl-2 was the lowest in the model group and the highest in the baicalein group while the mRNA level of pro-apoptotic gene Bax was the lowest in the baicalein group and the highest in the model group. The present results demonstrated that baicalein could reduce the occurrence of cirrhotic endotoxemia partly by reducing intestinal mucosal apoptosis.