control rats. With the progress of treatment, the body weights of rats in the model group continued to rise and began to decrease after the fourth week of treatment. The body weight of rats in each treatment group and the control group continued to increase during the treatment period of 8 weeks. Therefore, the drug may have produced a certain reversal effect on weight loss caused by the progression of hepatic fibrosis in rats. Among the treatment groups, the weight increase in the propranolol group was the most significant Compared with those in the control group, blood ALT, AST, and total bilirubin levels were significantly increased, but total protein and albumin levels were significantly decreased in the CCl4 group. Biejiaxiaozheng pills significantly reversed changes in the CCl4 group. And the high-dose Biejiaxiaozheng pills responded equally to propranolol In the control group, the hepatic lobule structure was normal. The hepatic cords were arranged in a regular manner, and necrosis, degeneration, and inflammatory cell infiltration were not observed. The fiber level was low. In the model group, the hepatic lobule structure was disrupted (Figure 3(a)), and the hepatic cords were arranged in a disorderly manner. Necrosis, degeneration, and inflammatory cell infiltration were observed, and interstitial hyperplasia was significant. Collagen fibers were wrapped around hepatic lobules to form apparent pseudolobules (Figure 3(b)). In the Biejiaxiaozheng pill group, the degree of pseudolobules, inflammatory cell infiltration, and necrosis were significantly improved compared with those in the model group. The therapeutic efficacy within the Biejiaxiaozheng pill group was slightly poorer than that in the propranolol group (Figure 3(c)). Serum TNF-α, IL-1β, and IL-6 levels in the CCl4 group were significantly increased compared with those in the control group. In the Biejiaxiaozheng pill group, TNF-α and IL-1β levels were significantly decreased, and IL-6 was downregulated; however, the effect of Biejiaxiaozheng pills on TNF-α was significantly weaker than that of propranolol, while the effects of Biejiaxiaozheng pills on IL-1β and IL-6 were not significantly different from those of propranolol, with values of 0.079 and 0.066, respectively 3.5. Effects of BJXZ Pills on Hepatic Inflammatory Factor Transcript Levels in Rats with Hepatic Fibrosis In liver tissues, the transcript levels of TNF-α, IL-1β, and IL-6 were significantly increased in the treatment groups. Biejiaxiaozheng pills significantly reduced the transcript levels of these three inflammatory factors, and the improvement effects of Biejiaxiaozheng pills were significantly better than those of propranolol. 3.6. Effects of BJXZ Pills on Blood MDA, SOD, GSH, and GPx Levels in Rats with Hepatic FibrosisIn the CCl4 group, plasma MDA level was significantly increased, showing that the degree of lipid peroxidation was higher in rats with hepatic fibrosis. However, Biejiaxiaozheng pills significantly decreased MDA levels and improved high lipid peroxidation in rats. At the same time, SOD, GSH, and GPx levels were significantly decreased, while MDA level was significantly increased in rats with hepatic fibrosis. However, Biejiaxiaozheng pills significantly increased SOD, GSH, and GPx levels, enhancing antioxidant activity in rats showed significantly upregulated Nrf2 and HO-1 expression in the Nrf2/HO-1 pathway and enhanced liver antioxidant activity; these effects were the most significant in the Biejiaxiaozheng pill group. Regarding the NF-κB pathway, p65 expression in the control group was significantly higher than that in the other groups, but there were no significant differences among the CCl4 and other groups. P-p65 expression in the CCl4 group was significantly higher than that in the other groups, but P-p65 expression in each treatment group was lower than that in the control group. P-p65 expression in the Biejiaxiaozheng pill group was the lowest, which inhibited the activation of the NF-κB pathway Every year, more than 2 million people worldwide die due to cirrhosis and liver cancer caused by viral hepatitis and alcoholic fatty liver disease [16]. Hepatic fibrosis is a type of hepatic scarring reaction that occurs after