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目的探讨二氮嗪预处理对幼龄大鼠深低温脑缺血/再灌注损伤脑保护作用。方法将3周龄SD大鼠90只随机分为假手术组、模型组及二氮嗪组,缺血/再灌注后1、6、24、72h和7d,建立深低温脑缺血/再灌注模型,采用免疫组织化学检测不同时点脑组织细胞色素C的蛋白表达,并观察脑组织病理变化。结果与假手术组比较,模型组于再灌注后6和24h显示明显的病理变化,其脑组织胞浆细胞色素C于灌注后6h后即明显升高(P<0.05),24h达到高峰(P<0.01)。二氮嗪组病理改变较轻,细胞色素C含量于再灌注后24和72h显著低于模型组(P<0.05)。结论二氮嗪预处理可抑制线粒体细胞色素C的释放,对幼龄大鼠深低温脑缺血/再灌注损伤具有一定脑保护作用。
Objective To investigate the neuroprotective effect of diazoxide preconditioning on brain injury following cryopreservation by cerebral ischemia-reperfusion in young rats. Methods Ninety-three-week-old SD rats were randomly divided into sham operation group, model group and diazoxide group. The rats were sacrificed at 1, 6, 24, 72 and 7 days after ischemia / reperfusion to establish deep hypothermic cerebral ischemia / reperfusion The protein expression of cytochrome C in brain tissue was detected by immunohistochemistry at different time points and pathological changes of brain tissue were observed. Results Compared with the sham group, the model group showed obvious pathological changes at 6 and 24 h after reperfusion. Cytochrome C in the cytoplasm of the model group increased significantly (P <0.05) 6 h after perfusion and peaked at 24 h (P <0.01). Diazoxide group pathological changes lighter, cytochrome C levels at 24 and 72h after reperfusion was significantly lower than the model group (P <0.05). Conclusion Diazoxide preconditioning can inhibit the release of cytochrome C from mitochondria and play a protective role on cerebral ischemia-reperfusion injury in young rats.