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目的研究希望Ⅱ号对被动吸烟小鼠肝脏的影响。方法 72只雄性昆明小鼠随机分为对照组,模型组,原花青素组,希望Ⅱ号(简称XwⅡ)低、中、高剂量组。对照组暴露于自然空气中,其余组别均造模,各组于造模后第16天开始给药,对照组、模型组每日灌胃双蒸水5.49 ml/kg,原花青素组每日灌胃原花青素16.47 ml/kg,XwⅡ低、中、高剂量组分别每日灌胃1.83 ml/kg,5.49 ml/kg,16.47 ml/kg希望Ⅱ号。45 d后取材,腹主动脉取血获得血清和肝脏,检测血清过氧化氢酶(CAT)活性,天冬氨酸氨基转移酶(AST),丙氨酸氨基转移酶(ALT)含量和肝组织总超氧化物歧化酶(TSOD),铜锌超氧化物歧化酶(Cu/Zn-SOD)活性及丙二醛(MDA)含量,肝脏组织学观察。形态计量肝细胞体积构成比、肝胶原纤维体积比。结果与对照组比较,模型组Cu/Zn-SOD、T-SOD、CAT活性降低(P<0.01),MDA、AST、ALT含量升高(P<0.01),肝细胞体积构成比增大(P<0.01),肝胶原纤维沉积增加(P<0.01)。与模型组比较,XwⅡ号低、中、高剂量组均能明显升高Cu/Zn-SOD、TSOD、CAT活力(P<0.01),明显降低MDA、AST、ALT含量(P<0.05,P<0.01),回降肝细胞体积构成比和胶原纤维沉积(P<0.01)。结论希望Ⅱ号保护被动吸烟小鼠肝脏损伤的机制可能是通过提高机体的抗氧化酶含量,调节氧化应激,维护抗氧化平衡,减轻淋巴细胞浸润,防治肝细胞水肿,延缓肝脏纤维化进程,从而保护肝脏。
Objective To study the effect of Hope II on the liver of passive smoking mice. Methods Seventy-two male Kunming mice were randomly divided into control group, model group, proanthocyanidin group, HopeⅡ (abbreviation XwⅡ) low, medium and high dose groups. The control group was exposed to natural air, the other groups were all modeled, each group began to be administered on the 16th day after the model was established. The control group and the model group were given 5.49 ml / kg of double distilled water daily, Gastro-proanthocyanidins 16.47 ml / kg, Xw Ⅱ low, medium and high dose groups were daily gavage 1.83 ml / kg, 5.49 ml / kg, 16.47 ml / kg Hope II. Serum and liver were obtained from the abdominal aorta after 45 days, and the activities of serum catalase (CAT), aspartate aminotransferase (AST), alanine aminotransferase (ALT) and liver tissue Total superoxide dismutase (TSOD), copper / zinc superoxide dismutase (Cu / Zn-SOD) activity and malondialdehyde (MDA) content in liver tissue were observed. Morphometry hepatocyte volume ratio, hepatic collagen fiber volume ratio. Results Compared with the control group, the activities of Cu / Zn-SOD, T-SOD and CAT decreased (P <0.01), the contents of MDA, AST and ALT increased <0.01), hepatic collagen deposition increased (P <0.01). Compared with the model group, the activities of Cu, Zn-SOD, TSOD and CAT in XwⅡ low, middle and high dose groups were significantly increased (P <0.01) and significantly decreased in MDA, AST and ALT groups (P < 0.01), volume composition ratio of hepatic cells and collagen deposition (P <0.01). Conclusion It is hoped that the mechanism of liver injury induced by No. II in passive smoking mice may be through increasing antioxidant enzyme content, regulating oxidative stress, maintaining antioxidant balance, reducing lymphocyte infiltration, preventing and treating hepatocyte edema, retarding hepatic fibrosis, Thus protecting the liver.