慢性乙醇中毒性周围神经病大鼠的氧化应激研究  

Study of Oxidative Stress in Chronic Alcoholism Peripheral Neuropathy

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作  者:谭春艳[1] 张霞[1] 王亚南[1] 程秀臻[1] 

机构地区:[1]潍坊医学院生理学教研室,山东潍坊261042

出  处:《潍坊医学院学报》2007年第3期224-225,共2页Acta Academiae Medicinae Weifang

摘  要:目的研究乙醇及其代谢产物的直接毒性作用所导致的大鼠坐骨神经氧化抗氧化平衡机制异常,以探讨慢性乙醇中毒性周围神经病的发病机制。方法建立慢性乙醇中毒性周围神经病大鼠模型,在实验开始后第8,12,16周分别测定其坐骨神经的谷胱甘肽(GSH)、谷胱甘肽过氧化物酶(GSH-PX)、丙二醛(MDA)值。结果乙醇灌胃第8周乙醇组大鼠GSH、GSH-PX含量增加显著,MDA量无变化;灌胃第12周GSH量下降,GSH-PX继续增加,MDA无明显变化;灌胃第16周GSH继续下降,GSH-PX酶活力骤降,MDA量明显增加。结论乙醇组大鼠坐骨神经中GSH,GSH-PX,MDA的动态变化反映了大鼠对乙醇损害的代偿性保护反应和最终抗氧化能力的降低导致了对组织的损害。Objective To study the direct toxic effect of alcohol and its metabolic product that induce the abnormal oxidative and antioxidative equilibrium mechanism in sciatic nerve of the rats,in order to investigate the pathogenetic mechanism of chronic alcoholism peripheral neuropathy.Methods To construct the model of chronic alcoholism peripheral neuropathy in rats,the contents of glutathione,glutathione peroxidase and malondialdehyde in sciatic nerve of rats were determined respectively on the eighth week,the twelfth week,and the sixteenthe week after experiment.Results The content of GSH and GSH-Px in sciatic nerve of the alcohol group increased obviously on the eighth week after intragastric administration,but the content of MDA did not change;The content of GSH decreased,and the content of GSH-Px continued to increase,the content of MDA did not change obviously;The content of GSH persisted in decreasing,and enzymatic vigor of GSH-PX decreased rapidly,but the content of MDA increased obviously on the sixth week after intragastric administration.Conclusion The changes of GSH,GSH-Px and MDA in sciatic nerve of alcoholism rats reflects the compensated protective reaction of rats on alcoholic impair and the loss of the ultima antioxidative ability which resulted in the pathological changes of the sciatic nerve.

关 键 词:慢性乙醇性周围神经病 丙二醛 谷胱甘肽 谷胱甘肽过氧化物酶 大鼠 

分 类 号:R338[医药卫生—人体生理学]

 

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