ABSTRACT
Objective: To observe the effect and mechanism of Jiedu Hugan decoction on drug-induced liver injury in rats by detecting serum liver function, serum biomarkers, inflammatory factors, macrophage inflammatory protein-2 (MIP-2) and macrophage inflammatory protein-1β (MIP-1β). Method: The rat model of drug-induced liver injury was induced by acetaminophen (1 g·kg-1) orally once daily for 30 days. The sixty male adult Wistar rats were divided into five groups, control group,model group,administered silybin group(44.1 mg·kg-1), Jiedu Hugan decoction high, medium and low dose groups (63,31.5,15.75 g·kg-1), normal group and model group were given normal saline gavage, and the other groups were given corresponding liquid gavage for 30 days. After the experiment, the abdominal aorta separation take blood serum aspartate amino transferase (AST), alanine aminotransferase (ALT), total bilirubin (TBIL), direct bilirubin (DBIL), malate dehydrogenase (MDH), enzyme for oxygen p1 (PON1) and glutamate dehydrogenase (GLDH), arginine (ARG), purine nucleotide phosphorylase (PNP), tumor necrosis factor-α(TNF-α), interleukin-6(IL-6) content. Pathological morphological changes of liver tissues were observed by hematoxylin-eosin (HE) staining. The protein expression of MIP-1β was observed by immunohistochemistry. The protein expression of MIP-2 was observed by single fluorescence immunohistochemistry, and the contents of TNF-α and IL-6 in liver homogenate were detected by enzyme-linked immunosorbent assay (ELISA). Result: Compared with normal group, levels of AST, ALT, DBIL, PON1, ARG, GLDH, MDH, PNP and TNF-α in model group were significantly increased (PPPPα in liver injury rats(PPβ protein expression, detoxification protect liver soup effect of the optimal dose group, the pathological morphology of liver cell dosage group were with different degree of protection. Conclusion: The effect of Jiedu Hugan decoction in medium dose group is better, and its mechanism may affect the chemotaxis of neutrophils induced by MIP-2 and MIP-1β by reducing the content of TNF-α, thus inhibiting the release of inflammatory factors and preventing inflammation.