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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。
Objective To study the changes of cerebral heme oxygenase-1 (HO-1), endogenous carbon monoxide (CO) and cyclic guanosine monophosphate (cGMP) in hypoxic-ischemic neonatal rats and explore the relationship between zinc protoporphyrin ) Of the therapeutic effect. Methods 7-day-old SD rats were randomly divided into sham-operation control group, hypoxic-ischemic group (HI) and hypoxia-ischemia + zinc protoporphyrin group (HI + Znpp). The content of COHb in blood and the activity of HO-1 in brain homogenate were determined by spectrophotometry. The level of cGMP in brain homogenate was determined by radioimmunoassay and the pathological changes of brain were observed. Results The levels of HO-1, cGMP and CO in HI + Znpp group were significantly higher than those in control group (P <0.01) , 12h were significantly lower than the HI group (P <0.01), but still higher than the control group (P <0.01). Histopathological examination showed that the HI group showed severe hypoxic-ischemic changes, most of the neuronal cell degeneration; and Znpp group of neurons degeneration less. Conclusion After HI, HO-1 activity in the brain is significantly increased, leading to increased endogenous CO and cGMP. Znpp can inhibit this pathophysiological process and reduce brain injury.