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目的探讨氧化损伤在高甘油三酯血症大鼠三酰甘油(TG)代谢紊乱中的作用机制。方法选取江苏建康职业学院实验室于2016年8月饲养的同一批次20只SD大鼠适应性饲养1周后,随机分为正常组和模型组,每组10只。正常组采用普通饲料饲喂,模型组大鼠采用高脂饲料法建立大鼠高三酰甘油血症模型,比较两组大鼠体质量、血脂指标〔TG、总胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)和游离脂肪酸(FFA)〕、丙二醛(MDA)、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-PX)及肝脏TG、TC含量。结果实验前两组大鼠体质量比较,差异无统计学意义(P>0.05);实验1、2、3、4周模型组大鼠体质量重于正常组(P<0.05)。实验2、4周模型组TG、TC、LDL-C及FFA水平高于正常组(P<0.05);实验4周模型组TG、TC、LDL-C及FFA水平高于2周(P<0.05);实验4周正常组TG、TC、LDL-C水平高于2周(P<0.05);实验2、4周正常组FFA水平比较,差异无统计学意义(P>0.05)。模型组MDA水平高于正常组,SOD、GSH-PX低于正常组(P<0.05)。模型组大鼠肝脏TG、TC含量高于正常组(P<0.05)。结论高甘油三脂血症大鼠TG代谢旺盛,氧化作用强烈,氧自由基产生过多,机体不能及时清除,造成氧化损伤,进而诱发动脉粥样硬化。
Aim To investigate the mechanism of oxidative damage in the metabolic disorder of triglyceride (TG) in hypertriglyceridemic rats. Methods Twenty SD rats of the same batch reared in the laboratory of Jiangsu Jiankang Vocational College in August 2016 were selected for one week and then randomly divided into normal group and model group with 10 rats in each group. The rats in the normal group were fed with common diet. The rats in the model group were fed with high fat diet to establish rat model of hypertriglyceridemia. The body weight, blood lipid (TG), total cholesterol (TC), low density lipoprotein LDL-C and FFA, MDA, SOD, GSH-PX and TG and TC in the liver were measured. Results There was no significant difference in body weight between the two groups before the experiment (P> 0.05). The body weight of model group was heavier than that of the normal group (P <0.05). The levels of TG, TC, LDL-C and FFA in model group at 2 and 4 weeks were higher than those in normal group (P <0.05). TG, TC, LDL-C and FFA in model group were higher than those at 2 weeks ). The level of TG, TC, LDL-C in the normal group was higher than that in the normal group at 4 weeks (P <0.05). There was no significant difference in the FFA levels between the normal group and the normal group at 2 and 4 weeks (P> 0.05). The level of MDA in the model group was higher than that in the normal group, and the levels of SOD and GSH-PX in the model group were lower than those in the normal group (P <0.05). The contents of TG and TC in liver of model group were higher than those of normal group (P <0.05). CONCLUSION: The TG in rats with hypertriglyceridemia is strongly metabolized, with strong oxidation and excessive production of oxygen free radicals. The body can not be cleared promptly, causing oxidative damage and then inducing atherosclerosis.