Protective Effects of Longhu Xingnao Granules on Neural Cells in a Rat Model of Cerebral Ischemia Reperfusion Injury via the MAPK Pathway
Objective:To investigate the neuroprotective effects of Longhu Xingnao Granules on cerebral ischemia-reperfusion injury(CIRI)in rats based on the MAPK pathway.Methods:The CIRI model was established using the middle cerebral artery occlusion(MCAO)method.Fifteen successfully modeled rats were randomly divided into the model group,Longhu Xingnao Granules group,and Ginaton group,with 5 rats in each group.An additional sham-operated group(5 rats)was also included.The Longhu Xingnao Granules group was administered 300 mg/kg Longhu Xingnao Granules by gavage,the Ginaton group received 150 mg/kg Ginaton,and the sham-operated and model groups were given an equal volume of saline,all for 5 days.Neurological function scores were assessed,brain infarct volume was measured using TTC staining,and MAPK,p-ERK,and p-CREB mRNA levels in brain tissue were detected using RT-PCR.Protein expressions of MAPK,p-ERK,p-CREB,Bcl-2,Bax,and Caspase-3 were determined by Western blot.Results:Compared with the sham-operated group,the model group showed significantly worse neurological damage,with increased neurological function scores,brain infarct volume,and Bax and Caspase-3 protein expressions(P<0.05),while MAPK,p-ERK,and p-CREB mRNA levels and MAPK,Bcl-2,p-ERK,and p-CREB protein expressions were significantly decreased(P<0.05).Compared with the model group,the Longhu Xingnao Granules and Ginaton groups showed significant reductions in neurological function scores,brain infarct volume,and Bax and Caspase-3 protein expressions(P<0.05),and significant increases in MAPK,p-ERK,p-CREB mRNA levels and MAPK,Bcl-2,p-ERK,and p-CREB protein expressions(P<0.05),with the Longhu Xingnao Granules group showing the most pronounced effects.Conclusion:Longhu Xingnao Granules improve neurological function scores,reduce brain infarct volume,and decrease apoptosis in CIRI model rats,exerting neuroprotective effects likely via the regulation of the MAPK pathway.
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维普
