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首页> 外文期刊>Life sciences >Protective effects of intraperitoneal injection of TAT-SOD against focal cerebral ischemia/reperfusion injury in rats.
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Protective effects of intraperitoneal injection of TAT-SOD against focal cerebral ischemia/reperfusion injury in rats.

机译：腹膜内注射TAT-SOD对大鼠局灶性脑缺血/再灌注损伤的保护作用。

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AIMS: The intracellular superoxide anion has been shown to be involved in brain injury. TAT-Superoxide dismutase (TAT-SOD) can be transduced across the cell membrane to scavenge superoxide. This protein's unique properties make it a promising therapeutic candidate to attenuate cerebral damage. In this study, we sought further the understanding of the fusion protein's cerebral protective effects and the mechanism which is exerted in these effects. MAIN METHODS: Male Sprague Dawley rats (n=100, 230+/-20 g) were divided randomly into five experimental groups: a sham group, a cerebral Ischemia/Reperfusion (I/R) group treated with saline (20 ml/Kg, i.p.), and three cerebral I/R groups treated with TAT-SOD (25 KU/ml/Kg, i.p.) at either 2h before I/R, 2h after I/R or 4h after I/R. Cerebral I/R injury was facilitated by inducing ischemia for two hours followed by 24h reperfusion. The levels of SOD, Malondialdehyde (MDA), and ATPase in cerebral tissues were determined. The apoptotic indexes were evaluated, and apoptosis genes were analyzed immunohistochemically. KEY FINDINGS: TAT-SOD treatment significantly increased cerebral SOD and ATPase activities, decreased MDA content, and remarkably reduced apoptosis indexes. TAT-SOD treatments 2h before or after I/R significantly reduced caspase-3 and bax proteins and boosted bcl-2 protein, while the treatment at 4h after I/R showed no influence on the three proteins. SIGNIFICANCE: TAT-SOD treatment effectively enhanced cerebral antioxidant ability, reduced lipid peroxidation, preserved mitochondrial ATPase and thus inhibited nerve cell apoptosis. The effective treatment window extended from 2h before to 2h after I/R.
机译：目的：已显示细胞内超氧化物阴离子参与脑损伤。 TAT-超氧化物歧化酶（TAT-SOD）可以通过细胞膜转导，以清除超氧化物。该蛋白质的独特性质使其成为衰减脑损伤的有希望的治疗候选者。在这项研究中，我们进一步了解融合蛋白的脑保护作用和施加在这些效果中的机制。主要方法：将雄性Sprague Dawley大鼠（n = 100,230 +/-20g）随机分为五个实验组：假目组，用盐水处理的脑缺血/再灌注（I / R）组（20ml / kg ，IP）和三个脑I / R基团在I / R之前的2小时内用TAT-SOD（25ku / ml / kg，IP）处理，在I / R后I / R或4小时后2小时。通过诱导缺血2小时后促进脑I / R损伤，然后再灌注24h再灌注。确定了SOD，丙二醛（MDA）和脑组织中的ATP酶的水平。评估凋亡指数，分析免疫组织化学分析细胞凋亡基因。主要发现：TAT-SOD处理显着增加了脑草皮和ATP酶活性，降低了MDA含量，并且显着降低了细胞凋亡指标。 TAT-SOD处理2h之前或之后I / R显着降低了Caspase-3和Bax蛋白并提高了Bcl-2蛋白，而I / R后的处理在4小时内对三种蛋白质没有影响。意义：TAT-SOD处理有效增强了脑抗氧化能力，降低了脂质过氧化，保存的线粒体ATP酶，从而抑制神经细胞凋亡。在I / R之后，有效的处理窗口从2小时延伸到2小时。

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