Plantamajoside reduces brain injury induced by cerebral ischemia-reperfusion in rats by regulating oxidative stress and inflammation
Objective:To investigate the effects of Plantamajoside(PMS)on hippocampal neuron damage in rats with cerebral ischemia/reperfusion(CI/R)and changes in oxidative stress and inflammation.Methods:The CI/R model of male SD rats was constructed,and the SD rats were randomly divided into five groups:control group,CI/R group,CI/R+PMS low,medium,and high dose groups(50 mg/kg,100 mg/kg,200 mg/kg).After 24 h reperfusion,brain function of each group was evaluated.Relevant protein expression was detected by immunoblotting.H-E staining was used to observe the changes of the pathological structure of the hippocampus.Nissl staining was used to observe the neuron injury.Superoxide dismutase(SOD)activity and malondialdehyde(MDA)content were detected with the kits.Results:Compared with the control group,the CI/R group of rats showed a significant increase in the number of platform jumping mistakes,brain water content,and neurological scores,while the new arm entries were significantly reduced.The neural cell structure in the hippocampus was significantly damaged,and the number of Nissl bodies was significantly reduced.The expression of caspase-3,caspase-9,and Bax/Bcl-2 was significantly upregulated.The SOD activity was significantly decreased,MDA content and NF-κB p65 phosphorylation level were significantly increased.Compared with CI/R,the PMS medium and high dose groups had significantly reduced number of platform jumping errors,brain water content and neurological scores,while the new arm entries were significantly increased.The damage to the neural cell structure in the hippocampus was weakened,and the number of Nissl bodies was increasesd.The expression of caspase-3,caspase-9,and Bax/Bcl-2 was significantly downregulated.The SOD activity was significantly enhanced,MDA content and NF-κB p65 phosphorylation level were significantly decreased.Conclusion:PMS can reduce the neuronal cell damage,reverse damaged brain function in CI/R rats,and the mechanism may be due to the inhibition of NF-κB p65 activation and alleviation of oxidative stress.
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