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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：TAT-SOD腹腔注射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：已经证明细胞内超氧阴离子与脑损伤有关。 TAT-超氧化物歧化酶（TAT-SOD）可以跨细胞膜转导以清除超氧化物。这种蛋白质的独特性质使其成为减轻脑损伤的有前途的候选治疗药物。在这项研究中，我们寻求进一步了解融合蛋白的脑保护作用以及在这些作用中发挥作用的机制。主要方法：雄性Sprague Dawley大鼠（n = 100，230 +/- 20 g）随机分为五个实验组：假手术组，脑缺血/再灌注（I / R）组，用生理盐水（20 ml / Kg）治疗，ip）和三个接受TAT-SOD（25 KU / ml / Kg，ip）的脑I / R组，分别在I / R前2h，I / R后2h或I / R后4h进行。诱导缺血2小时，然后再灌注24 h可促进脑I / R损伤。测定了脑组织中的SOD，丙二醛（MDA）和ATPase的水平。评估细胞凋亡指数，并免疫组织化学分析凋亡基因。主要发现：TAT-SOD处理可显着增加脑组织SOD和ATPase活性，降低MDA含量，并显着降低细胞凋亡指数。在I / R之前或之后2h的TAT-SOD处理显着降低了caspase-3和bax蛋白并增强了bcl-2蛋白，而在I / R之后4h的处理对这三种蛋白没有影响。意义：TAT-SOD治疗可有效增强脑部抗氧化能力，减少脂质过氧化作用，保持线粒体ATPase并因此抑制神经细胞凋亡。有效治疗窗口从I / R前2h延长到I / R后2h。

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