Effect of polydatin on expression of p53 and Notch1 in brain tissue of ischemic cerebrovascular disease

F Y. Chen; X Y. Fang; H. Zhang

doi:10.54517/jbrha5036

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Effect of polydatin on expression of p53 and Notch1 in brain tissue of ischemic cerebrovascular disease

F Y. Chen, X Y. Fang, H. Zhang

Article ID: 5036
Vol 32, Issue 1, 2018

DOI: https://doi.org/10.54517/jbrha5036

Received: 11 March 2018; Accepted: 11 March 2018; Available online: 11 March 2018; Issue release: 11 March 2018

Abstract

Secondary injury of brain tissue following cerebral infarction exhibits a complicated pathogenesis that is attributed to the induction of apoptosis and inflammatory response. The present study aimed to investigate the polydatin neuroprotective effects and their mode of action in cerebral ischemic injury. A total of 80 healthy adult male Sprague-Dawley rats were randomly divided into a Sham operated group, a permanent middle cerebral artery occlusion (MCAO) group, a Polydatin low dose group and a Polydatin high dose group. A total of 20 rats were used in each group. The right MCAO model of rats was established using the modified Longa suture method. The animals in the intervention group were injected intraperitoneally with 12.5mg/kg and/or 50mg/kg of polydatin following infarction. The expression levels of p53 and Notch 1 were measured by immunohistochemical techniques. The degree of left limb hemiplegia in the MCAO group was different compared with that of the low and high dose group of polydatin. The score for the neurological function in the high-dose group of polydatin was lower than that in the MCAO group (High vs MCAO: 2.4±0.31 vs 3.9±0.23, P less than0.05). The results indicated that high dose polydatin could reduce brain edema following cerebral infarction and improve the behavioral score in rats

Keywords

polydatin;brain protection;cerebral infarction;p53;Notch 1

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Medical Genetics, University of Torino Medical School, Italy

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Department of Biomedical, Surgical and Dental Sciences, University of Milan, Italy

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2025-02-01

Notice of Change in Publication Schedule

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