缺血预处理经抑制线粒体释放细胞色素C减轻大鼠海马神经元缺血再灌注损伤

Ischemia preconditioning reduces ischemia/reperfusion injury of the hippocampal neurons by inhibiting the release of cytochrome c from mitochondria in rats

目的:探讨线粒体细胞色素C的释放在缺血预处理(IPC)保护大鼠海马神经元缺血再灌注损伤中的作用。方法:动物随机分为单纯缺血再灌组(IR组)、IPC加缺血再灌组(IPC+IR组)和对照组。HE染色观察海马CA1区神经元的组织形态学变化;TUNEL染色检测该区神经元凋亡;免疫组化测定该区神经元细胞色素C的表达。结果:IPC+IR组海马CA1区神经元存活数显著多于IR组,凋亡细胞数显著低于IR组,细胞色素C的释放明显少于IR组(P均<0.001)。结论:IPC可经阻止线粒体释放细胞色素C抑制凋亡的发生,对海马CA1区神经元缺血再灌损伤起保护作用。

Objective： To investigate the role of the release of cytochrome c from mitochondria in the protective process of hippocampal neurons against ischemia/reperfusion injury by cerebral ischemic preconditioning （IPC） in rots. Methods： Rats were randomly divided into three groups： an ischemia/reperfusion group （IR）, an ischemic preconditioning ＋ ischemia/reperfusion group （IPC ＋ IR）, and the control group. Histological changes in the neurons of the hippocampal CA1 region were obtained by HE staining. The apoptotic neurons were counted with TUNEL staining and the release of cytochrome c from the mitochondria were determined with immunohistochemistry in the same brain area. Results： Compared with the IR group, cerebral ischemic preconditioning can increase the number of surviving neurons in the hippocampal CA1 region（ P 〈 0.001）, markedly reduce the number of apoptotic pyramidal neurons（ P 〈 0.001）, and inhibit the release of cytochrome c from mitochondria. Conclusion： Cerebral ischemic preconditioning （IPC） can protect the hippocampla neurons against ischemia/reperfusion injury by reducing the release of cytochrome c from mitochondria and inhibiting the apoptosis.