2002Yiyao daobaoRequires access

Effects of Melatonin on Focal Cerebral Ischemia in Rats

Ming Zhang

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Abstract

Objective:To explore the protective effects and mechanism of melatonin on permanent focal cerebral ischemia. Methods:Brain ischemia was studied with 20 models of right middle cerebral artey occlusion (MCAO) for 30 min or 6 h or 24 h in rats. Brain damage was measured at the infarct area about the content of MDA and NO, and the activity of NOS. Moreover, alteration of ultrastructure was observed by transmission electronic microscope. Results:30 min after the onset of cerebral ischemia, the activity of NOS and the content of MDA and NO were increased; and 6 h after cerebral ischemia, the content of MDA progressively became stable, but the activity of NOS and the content of NO were decreased; 24 h after that, the activity of NOS and the content of NO were increased again. In comparison with the model group, Melatonin significantly diminished the infarct area and decreased the content of MDA during the course. It increased the activity of NOS and the content of NO in 30 min after cerebral ischemia and decreased them in 6 h and 24 h after cerebral ischemia. It also improved the pathologic change of the ultrastructure. Conclusion:Melatonin has a certain therapeutic effect on focal cerebral ischemia in rats, the mechanism of which may be associated with the decrease of the content of NO, the activity of NOS and neuronal apoptosis.

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Objective:To explore the protective effects and mechanism of melatonin on permanent focal cerebral ischemia. Methods:Brain ischemia was studied with 20 models of right middle cerebral artey occlusion (MCAO) for 30 min or 6 h or 24 h in rats. Brain damage was measured at the infarct area about the content of MDA and NO, and the activity of NOS. Moreover, alteration of ultrastructure was observed by transmission electronic microscope. Results:30 min after the onset of cerebral ischemia, the activity of NOS and the content of MDA and NO were increased; and 6 h after cerebral ischemia, the content of MDA progressively became stable, but the activity of NOS and the content of NO were decreased; 24 h after that, the activity of NOS and the content of NO were increased again. In comparison with the model group, Melatonin significantly diminished the infarct area and decreased the content of MDA during the course. It increased the activity of NOS and the content of NO in 30 min after cerebral ischemia and decreased them in 6 h and 24 h after cerebral ischemia. It also improved the pathologic change of the ultrastructure. Conclusion:Melatonin has a certain therapeutic effect on focal cerebral ischemia in rats, the mechanism of which may be associated with the decrease of the content of NO, the activity of NOS and neuronal apoptosis.

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Available abstract

Objective:To explore the protective effects and mechanism of melatonin on permanent focal cerebral ischemia. Methods:Brain ischemia was studied with 20 models of right middle cerebral artey occlusion (MCAO) for 30 min or 6 h or 24 h in rats. Brain damage was measured at the infarct area about the content of MDA and NO, and the activity of NOS. Moreover, alteration of ultrastructure was observed by transmission electronic microscope. Results:30 min after the onset of cerebral ischemia, the activity of NOS and the content of MDA and NO were increased; and 6 h after cerebral ischemia, the content of MDA progressively became stable, but the activity of NOS and the content of NO were decreased; 24 h after that, the activity of NOS and the content of NO were increased again. In comparison with the model group, Melatonin significantly diminished the infarct area and decreased the content of MDA during the course. It increased the activity of NOS and the content of NO in 30 min after cerebral ischemia and decreased them in 6 h and 24 h after cerebral ischemia. It also improved the pathologic change of the ultrastructure. Conclusion:Melatonin has a certain therapeutic effect on focal cerebral ischemia in rats, the mechanism of which may be associated with the decrease of the content of NO, the activity of NOS and neuronal apoptosis.

Key concepts: Melatonin, Ischemia, Medicine, Internal medicine, Endocrinology, Occlusion, Anesthesia

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