论文部分内容阅读
目的:研究F1013对D-氨基半乳糖(D-Gal N)及脂多糖(LPS)所致大鼠急性肝损伤模型的治疗作用,并对其机制进行初步探讨。方法:60只雄性W istar大鼠随机分成对照组、模型组、阳性药组(N-乙酰半胱氨酸,155 m·gkg-1)和F1013给药组(5,2.5,1.25 m·gkg-1)。除对照组外,各组大鼠均腹腔注射D-GalN/LPS建立大鼠急性肝损伤模型,造模后2 h,阳性药组和F1013给药组分别腹腔注射NAC和F1013,其余组腹腔注射等体积生理盐水。造模后10 h,留取血清和肝组织,用全自动生化分析仪检测血清丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)和总胆红素(T-Bil)含量;用苏木素-伊红(HE)染色,观察肝组织病理学变化;采用流式细胞学技术和原位末端标记(TUNEL)法检测肝细胞凋亡情况。结果:在D-GalN/LPS诱导大鼠急性肝损伤模型,各剂量F1013均明显改善肝脏病理组织损伤;明显降低血清ALT,AST,T-Bil水平及肝细胞凋亡率(P<0.05)。结论:F1013对D-GalN/LPS所致大鼠急性肝损伤具有较好的治疗作用,其机制可能与抑制肝细胞异常凋亡有关。
Objective: To investigate the therapeutic effect of F1013 on acute liver injury induced by D-galactosamine (L-Gal) and lipopolysaccharide (LPS) in rats and its mechanism. Methods: Sixty male Wistar rats were randomly divided into control group, model group, positive group (N-acetylcysteine, 155 m · g kg -1) and F1013 group (5, 2.5 and 1.25 m · g kg -1). In addition to the control group, rats were injected intraperitoneally with D-GalN / LPS to establish the model of acute liver injury in rats. After 2 h, the rats in the positive group and the F1013 group were intraperitoneally injected with NAC and F1013, Equal volume of saline. Serum ALT, AST and T-Bil were detected by automatic biochemical analyzer after 10 h of modeling. Hematoxylin and eosin (HE) staining was used to observe the histopathological changes of liver tissues. The apoptosis of hepatocytes was detected by flow cytometry and TUNEL. Results: In the model of acute liver injury induced by D-GalN / LPS, all the doses of F1013 significantly improved liver pathological tissue injury; significantly reduced the levels of serum ALT, AST, T-Bil and the rate of hepatocyte apoptosis (P <0.05). Conclusion: F1013 has a good therapeutic effect on acute liver injury induced by D-GalN / LPS in rats, which may be related to the inhibition of abnormal apoptosis of hepatocytes.