摘要
目的 研究一氧化碳对局灶性脑缺血脑组织脂质过氧化物及Na+ K+ ATP酶的影响 ,试图从亚细胞水平阐明CO对脑组织保护作用的机理。方法 将SD大鼠随机分为三组 (n =6 ) ,使用HO诱导剂、HO抑制剂腹腔注射为实验组 ,等量生理盐水作为对照组腹腔注射 ,12h后制成MCAO模型。栓塞后 2 4h检测CO浓度、脂质过氧化及Na+ K+ ATP酶活性。结果 与对照组相比 ,HO诱导剂组CO浓度明显升高 ,MDA减少 ,SOD及Na+ K+ ATP酶增高 (各为P <0 .0 1、P <0 .0 1、P <0 .0 5、P <0 .0 5 ) ,而HO抑制剂组CO浓度明显降低 ,MDA增加 ,SOD及Na+ K+ ATP酶活性降低 (各为P <0 .0 0 1、P <0 .0 5、P <0 .0 5、P <0 .0 5 )。HO诱导剂、HO抑制剂对非栓塞侧脑组织脂质过氧化物及Na+ K+ ATP酶的活性没有影响 (P >0 .0 5 )。结论 CO是一种信使分子 ,通过减少自由基、增加SOD及Na+ K+
Objective To explore the mechanism of CO in brain protection by eveluating the effect to MDA and activities of SOD\,Na + K + ATPase following local cerebral ischemia in SD rats.Methods SD rats were divided into three groups randantly, which included hemin and ZnPP group and saline group as control. Salin\,hemin and ZnPP were injected intra peritoneal respectively at twelve hour before infarction, twenty four hours after infarction, the concentration of CO\,MDA\,activities of SOD and Na + K + ATPase were examined. Results The concentration of CO in blood\,activities of SOD and Na + K + ATPase was higher and MDA was lower in Hemin group compaired saline group, but activities of SOD and Na + K + ATPase was lower, MDA was higher in ZnPP group compaired saline group. There was significant difference between them. Hemin and ZnPP had no effect on MDA activities of SOD and Na + K + ATPase in noninfarcted side ( P > 0.05 ). Conclusion Carbon monoxide has brain protection effect as a messenger gas molecular through reducing MDA and promoting activities of SOD and Na + K + ATPase when its concentration has elevated.
出处
《卒中与神经疾病》
2002年第2期67-70,共4页
Stroke and Nervous Diseases
