Effects of melatonin on oxidization injury and on expression of P53 protein during ischemia-reperfusion in brain tissue of rats
Li Li
Abstract
Li Li
Abstract
The aim of this paper is to figure out the mechanism of the neuro protection effect of melatonin(MT) in the global cerebral ischemia reperfusion rats. After four vessel occlusion(20 min), rats with global cerebral ischemia were divided into groups. ①MT 2.5 or 10 mg·kg -1 was injected ip at the beginning of reperfusion. After 60 min reperfusion rats were sacrificed and brains were taken out to determine the activities of glutathione peroxidase(GSH Px) and superoxide dismutase(SOD), and the content of malondialdehyde(MDA). ②Another groups of rats were injected ip with MT 2.5 or 10 mg·kg -1 repeatedly at 0, 1, 2 and 6 h after the commence of reperfusion. Brain tissues were taken at 24 h after reperfusion and the expressions of P53 protein in neurons of hippocampal CA1 were measured by immunohistochemistry method. The results showed that both MT 2.5 and 10 mg·kg -1 increased the activities of antioxidant enzymes such as GSH Px and SOD, and also reduced the content of MDA in brain tissues at 1 h reperfusion after 20 min global cerebral ischemia. Both of the dosages decreased P53 immuno reactivity in neurons of hippocampal CA1 at the end of 24 h reperfusion. The results suggest that the protection of MT on brain against cerebral injury during ischemia reperfusion be oweing to at least two mechanisms, ①increasing activities of antioxidant enzymes SOD and GSH Px, reducing injury induced by lipid peroxidation, and ②inhibiting the expression of P53 protein.
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The aim of this paper is to figure out the mechanism of the neuro protection effect of melatonin(MT) in the global cerebral ischemia reperfusion rats. After four vessel occlusion(20 min), rats with global cerebral ischemia were divided into groups. ①MT 2.5 or 10 mg·kg -1 was injected ip at the beginning of reperfusion. After 60 min reperfusion rats were sacrificed and brains were taken out to determine the activities of glutathione peroxidase(GSH Px) and superoxide dismutase(SOD), and the content of malondialdehyde(MDA). ②Another groups of rats were injected ip with MT 2.5 or 10 mg·kg -1 repeatedly at 0, 1, 2 and 6 h after the commence of reperfusion. Brain tissues were taken at 24 h after reperfusion and the expressions of P53 protein in neurons of hippocampal CA1 were measured by immunohistochemistry method. The results showed that both MT 2.5 and 10 mg·kg -1 increased the activities of antioxidant enzymes such as GSH Px and SOD, and also reduced the content of MDA in brain tissues at 1 h reperfusion after 20 min global cerebral ischemia. Both of the dosages decreased P53 immuno reactivity in neurons of hippocampal CA1 at the end of 24 h reperfusion. The results suggest that the protection of MT on brain against cerebral injury during ischemia reperfusion be oweing to at least two mechanisms, ①increasing activities of antioxidant enzymes SOD and GSH Px, reducing injury induced by lipid peroxidation, and ②inhibiting the expression of P53 protein.
Key concepts: Malondialdehyde, Lipid peroxidation, Ischemia, Reperfusion injury, Melatonin, Superoxide dismutase, Glutathione peroxidase, Chemistry