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目的:观察玉郎伞多糖(YLSP)对环磷酰胺(CTX)致小鼠肝损伤的治疗作用并探讨其作用机制。方法:将小鼠随机分为正常对照组(NC),肝损伤模型组(CTX),阳性对照组(联苯双酯,BPDC),YLSP(玉郎伞多糖)高、中、低剂量组。除正常对照组外,其余各组小鼠每天腹腔注射CTX 40 mg·kg-1,共7 d,建立小鼠肝损伤模型。造模后连续灌胃7 d,观察YLSP对小鼠血清谷氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)、谷胱甘肽(GSH)、谷胱甘肽过氧化物酶(GSH-Px)、超氧化物歧化酶(SOD)和丙二醛(MDA)活性,苏木精-伊红(HE)染色观察小鼠肝脏组织病理学改变。结果:与模型组比较,YLSP各剂量组均能降低小鼠血清中ALT、AST活性及肝组织中MDA的含量;同时能增加肝组织中GSH含量及SOD和GSH-Px活性(P<0.05或P<0.01);HE染色结果显示YLSP能减轻CTX所致的肝组织变性、坏死程度,可减轻小鼠肝组织病理损伤程度。结论:YLSP对CTX所致小鼠肝损伤具有良好的保护作用。
Objective: To observe the therapeutic effect of YLSP on liver injury induced by cyclophosphamide (CTX) in mice and its mechanism. Methods: The mice were randomly divided into normal control group (NC), liver injury model group (CTX), positive control group (Bifendate, BPDC), YLSP high, medium and low dose groups. Except the normal control group, the mice in other groups were injected intraperitoneally with CTX 40 mg · kg-1 for 7 days to establish a mouse model of liver injury. After continuous intragastric administration for 7 days, the effects of YLSP on serum glutamate aminotransferase (ALT), aspartate aminotransferase (AST), glutathione (GSH), glutathione peroxidation The activities of GSH-Px, SOD and MDA were detected. The pathological changes of liver were observed by hematoxylin-eosin staining. Results: Compared with the model group, each dose of YLSP could reduce the activity of ALT and AST in serum and the content of MDA in liver tissue, increase the content of GSH and the activities of SOD and GSH-Px in liver (P <0.05 or P <0.01). The results of HE staining showed that YLSP could reduce the degree of liver degeneration and necrosis caused by CTX, and alleviate the pathological damage of liver in mice. Conclusion: YLSP has a good protective effect on CTX induced liver injury in mice.