缺氧缺血新生鼠脑内血红素氧化酶-1和一氧化碳的变化(英文)

Change of heme oxygnease-1and endogenous carbon monoxide in the brain of newborn hypoxic ischmia rats

目的研究新生大鼠缺氧缺血时脑内血红素氧化酶-1(HO-1)和内源性一氧化碳(CO)及环化鸟苷酸(cGMP)的变化,探讨锌原卟啉(Znpp)的治疗作用。方法7dSD大鼠随机分为假手术对照组,缺氧缺血组(HI)及缺氧缺血+锌原卟啉组(HI+Znpp)。利用分光光度法测定血COHb含量和脑匀浆HO-1活性;放免法测定脑匀浆cGMP水平,并观察脑病理改变。结果HI组在1,4,12hHO-1、cGMP、CO水平与对照组比明显升高(P<0.01),在12h达到高峰;HI+Znpp组HO-1、cGMP、CO水平在1,4,12h均明显低于HI组(P<0.01),但仍高于对照组(P<0.01)。脑组织病理检查可见HI组呈重度缺氧缺血改变,多数神经元细胞肿胀变性;而Znpp组神经元变性者少。结论HI后脑内HO-1活性明显增高导致内源性CO和cGMP增高,Znpp可阻抑这一病理生理过程,减轻脑损伤。

Aim To study the change of heme oxygnease-1(HO-1)and endogenous carbon monoxide(CO)on hypoxia-ischemia brain damage(HIBD)in newborn rats and the therapeutic e ffect of the Znpp on HIBD.Method7d SD rats were divided into control gro up,hypoxic-ischemia group(HI )and hy-poxic-ischemia +Znpp group(HI +Znpp)at random.HO-1activity,cGMP level in the brain and carbon monoxide level in blood were observed respectively at 1,4,12and 24h after hypoxic-ischem ia by using spectrophotometry etc.Results HO-1activity,CO and cGMP level of HI group were significant higher than those of control groups a t 1,4,12h (P<0.01);In HI,neurons were damaged severely,Znpp could antago nize the about-mentioned pathological changes effectively.Conclusion In HIBD,the increased HO-1activity re-sulted in increase of endogenous CO t hat can enhance cGMP;Znpp may protec t nerve cell from damage by preventing HO-1activity resulted in decrease o f endogenous CO.HO-CO-cGMP system ma y play an important role in the pathogenesis of HIBD.