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[新生大鼠缺氧缺血脑组织中神经元型一氧化氮合酶的表达及神经元型一氧化氮合酶抑制剂7-硝基吲唑的脑保护作用]

[Expression of neuronal nitric oxide synthase in brain tissue of hypoxic-ischemic neonatal rat and the cerebral protective effect of neuronal nitric oxide synthase inhibitor 7-nitroindazole].

作者信息

Chu Gui-lan, Xin Yue, Cheng Ji, Bi Shu-ying

机构信息

Department of Pediatrics, Tianjin Medical University General Hospital, Tianjin 300052, China.

出版信息

Zhonghua Yi Xue Za Zhi. 2004 Jan 17;84(2):156-8.

PMID:14990136
Abstract

OBJECTIVE

To explore the effect of nNOS and its selective inhibitor 7-NI in neonatal rats with hypoxic-ischemic brain damage (HIBD).

METHODS

The model of HIBD in neonatal rat was made and the expression of nNOS mRNA was measured at different time points and compared with the control group. The levels of NOS, NO, MDA, SOD were also assayed at different time points after aderministering 7-NI, and compared with the HIBD group and the control group. In addition, we observed the degree of apoptosis after 24 h of HIBD.

RESULTS

Expression of nNOS mRNA was higher at 2 h and 6 h after hypoxia than those in the control group (P < 0.05) and reached more at 6 h (P < 0.05). Concentrations of NOS, NO, MDA increased after HIBD, but concentration of SOD decreased (P < 0.01); 7-NI reduced the levels of NOS, NO, MDA, and level of SOD was higher than those in the HIBD group (P < 0.05). There was no apoptosis in the control group, 7-NI could effectively inhibit the degree of apoptosis after HIBD (P < 0.001).

CONCLUSION

nNOS has an important role in the pathogenesis of neonatal rats with HIBD, its specific inhibitor 7-NI can protect brains from hypoxic-ischemic damage through anti-oxidation and prohibiting apoptosis.

摘要

目的

探讨神经元型一氧化氮合酶(nNOS)及其选择性抑制剂7-硝基吲唑(7-NI)对新生大鼠缺氧缺血性脑损伤(HIBD)的影响。

方法

制作新生大鼠HIBD模型,检测不同时间点nNOS mRNA的表达,并与对照组比较。给予7-NI后,检测不同时间点一氧化氮合酶(NOS)、一氧化氮(NO)、丙二醛(MDA)、超氧化物歧化酶(SOD)水平,并与HIBD组和对照组比较。此外,观察HIBD 24小时后的细胞凋亡程度。

结果

缺氧后2小时和6小时nNOS mRNA表达高于对照组(P<0.05),6小时时更高(P<0.05)。HIBD后NOS、NO、MDA浓度升高,SOD浓度降低(P<0.01);7-NI降低了NOS、NO、MDA水平,SOD水平高于HIBD组(P<0.05)。对照组无细胞凋亡,7-NI可有效抑制HIBD后的细胞凋亡程度(P<0.001)。

结论

nNOS在新生大鼠HIBD发病机制中起重要作用,其特异性抑制剂7-NI可通过抗氧化和抑制细胞凋亡保护脑免受缺氧缺血损伤。

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