It has also been demonstrated that cytokine blockade with anti-TNFa monoclonal antibody can decrease the incidence of BT in Yohimbine-Hydrochloride cirrhotic rats with ascites, and the integrity of intestinal barrier can be preserved in the IL-6 knockout mice. In addition, Yang et al showed that salvianolate inhibited the expression of TNF-a and IL-6 and ameliorated intestinal mucosal injury of cirrhotic rats. In agreement with previous studies, we observed that expression level of NF-kB p65, TNF-a, and IL-6 was significantly reduced in animals that received oxymatrine treatment. Among the pro-inflammatory mediators, TNF-a has a significant role in the initiation, development and Neosperidin-dihydrochalcone worsening of intestinal barrier dysfunction. Previous studies have shown that TNF-a is an important mediator of bacterial invasion, and it can initiate the production of cytokines such as IL-6 and IFN-c, which can exacerbate the intestinal epithelial barrier injury. In clinic settings, the serum level of TNF-a and IL-6 are significantly increased in cirrhotic patients. In this study, the altered intestinal epithelial barrier function in rats with liver cirrhosis was observed with an increase in TNF-a and IL-6 expression levels in small intestine. These observations suggest that oxymatrine may directly inhibit inflammation response contributing to the restoration of disrupted intestinal epithelial barrier function in cirrhotic rats. Therefore, suppressing the activation of NF-kB signaling pathway and blocking the inflammation response may present new therapeutic strategies for the intestinal epithelial barrier injury. Additionally, in order to further evaluate the improvement of intestinal mucosal barrier function after the treatment of oxymatrine, we detected the plasma level of endotoxin. It has been reported that endotoxin can activate toll-like receptor 4, initiate inflammatory response, stimulate macrophages and monocytes, and enhance the production of pro-inflammatory cytokines such as TNF-a and IL-6. In our study, the plasma endotoxin level was significantly increased in nontreatment group.