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Fujian, China

Ye N.,Fuzhuo University | Ye N.,Fuzhuo University | Liu S.,Fuzhuo University | Liu S.,Fuzhuo University | And 4 more authors.
Life Sciences | Year: 2011

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 2 h before I/R, 2 h after I/R or 4 h after I/R. Cerebral I/R injury was facilitated by inducing ischemia for two hours followed by 24 h 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 2 h before or after I/R significantly reduced caspase-3 and bax proteins and boosted bcl-2 protein, while the treatment at 4 h 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 2 h before to 2 h after I/R. © 2011 Elsevier Inc. All rights reserved. Source

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