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目的:探讨退黄汤(THT)联合熊去氧胆酸(UDCA)对α-异硫氰酸萘酯(ANIT)诱导大鼠肝损过程保护作用及机制。方法:选取Sprague-Dawley(SD)大鼠84只,设立空白组6只,对剩余78只在0 h时间点均以ANIT 100 mg/kg予以灌胃造成急性肝损伤,在肝损后24 h取6只处死留取标本(肝损24 h组),然后分为生理盐水组(18只,9 mL/kg体重的生理盐水灌胃)、UDCA组(18只,20 mg/kg体重的UDCA溶液灌胃)、THT组(18只,20 mL/kg体重的THT灌胃)、UDCA/THT组(18只,20 mg/kg体重的UDCA和20 mL/kg体重的THT联合灌胃),各组分别在肝损造模后48 h、72 h、96 h处死6只大鼠。所有大鼠处死留取血清和肝组织,生化仪检测血清谷丙转氨酶(ALT)、谷草转氨酶(AST)、总胆红素(TBI)、总胆汁酸(TBA),酶联免疫吸附法(ELISA)检测血清白介素-10(IL-10)白介素-6(IL-6)肿瘤坏死因子-α(TNF-α),实时荧光定量PCR检测肝组织多药耐药相关蛋白2(Mrp2)mRNA,苏木素-伊红(HE)染色观察肝组织炎症活动度。结果:UDCA和THT在降低血清ALT、AST、TBI、TBA、IL-6、TNF-α和提升血清IL-10及肝组织Mrp2 mRNA均存在明显的主效应(P<0.01),两药在调控血清TBI、IL-6、TNF-α、IL-10及肝脏Mrp2 mRNA均存在明显交互协同作用(P<0.01或P<0.05)。HE染色显示联合用药组96 h肝组织炎性程度轻于单药组及生理盐水组。结论:UDCA和THT联合降低了ANIT诱导的肝损作用可能和两药联合作用调控血清细胞因子及肝脏Mrp2表达有关。
Objective: To investigate the protective effect and mechanism of decoction of the yellow (THT) combined with ursodeoxycholic acid (UDCA) on hepatic injury induced by α-isothiocyanate (ANIT) in rats. Methods: Totally 84 Sprague-Dawley (SD) rats were selected and 6 rats in the blank group were established. Acute liver injury was induced by feeding 100 mg / kg of ANIT to the remaining 78 rats at 0 h time point. Six rabbits were sacrificed for 24 h and then divided into saline group (18 rats, 9 mL / kg body weight normal saline), UDCA group (18 rats, 20 mg / kg body weight UDCA (N = 18, 20 mL / kg body weight THT), UDCA / THT (18 mg / kg body weight UDCA and 20 mL / kg body weight THT) Six rats in each group were sacrificed at 48 h, 72 h and 96 h after hepatic injury. All the rats were killed and serum and liver tissues were collected. Serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), total bilirubin (TBI), total bile acid (TBA) and enzyme-linked immunosorbent assay (TNF-α) in serum and interleukin-10 (IL-6) and real-time fluorescent quantitative PCR (MRP-2) Eosin (HE) staining was used to observe the activity of liver tissue. Results: UDCA and THT had significant main effects (P <0.01) in decreasing serum ALT, AST, TBI, TBA, IL-6 and TNF-α and promoting serum IL-10 and Mrp2 mRNA Serum TBI, IL-6, TNF-α, IL-10 and Mrp2 mRNA had significant interaction and synergy (P <0.01 or P <0.05). Hematoxylin-eosin staining showed that the inflammatory degree of liver tissue in combination group was lighter than that in monotherapy group and normal saline group at 96 h. Conclusion: UDCA combined with THT can reduce the hepatic damage induced by ANIT, which may be related to the combined effect of the two drugs in regulating serum cytokines and Mrp2 expression in the liver.