| Objectives: Pachymic acid(PA)from the medicinal fungus Poria has multiple pharmacological potentials.However,there are no reports on the effect of PA on cerebral ischemia/reperfusion(IR)injury.This study aimed to investigate the mechanism of PA on brain IR injury in rats.Methods: The effects of PA on cerebral ischemia-reperfusion infarct size,brain water content and neurological symptoms of experimental animals were evaluated.The degree of neurological impairment was evaluated according to the scoring standard of neurological impairment in MCAO rats.The rat brain slices were photographed with a digital camera,and the cerebral infarction area of the experimental animals was measured with the image analysis software Image J,and the brain water content was measured by weighing.Nissl staining was used to observe the injury of ischemic brain neurons in rats after IR.TUNEL staining was used to observe the apoptosis of ischemic brain neurons after IR.Western blotting detection of PA on PI3K/Akt signaling pathway components,p-PTEN(Ser380),p-PDK1(Ser241),p-Akt(Ser473),pc-Raf(Ser259),p-BAD(Ser136),Cleaved caspase effect on protein expression.Results: PA significantly increased cerebral blood flow in rats after IR,decreased infarct volume and cerebral water content,decreased neurological function scores,significantly reduced neuronal damage and significantly reduced neuronal apoptosis in rats after IR.The effect of PA on rat IR can be abolished by LY294002.In addition,PA significantly up-regulated the protein expression of p-PTEN(Ser380),p-PDK1(Ser241),p-Akt(Ser473),pc-Raf(Ser259)and p-BAD(Ser136),and down-regulated the protein expression of Cleaved caspase express.LY294002 can reverse the effect of PA on the expression of PI3K/Akt signaling pathway-related proteins after IR in rats.PA has obvious neuroprotective effect on brain IR injury and neuronal apoptosis.Conclusion: PA can reduce cerebral ischemia-reperfusion injury and the expression of caspase 3 by activating PI3K/Akt signaling pathway.The PI3K/Akt signaling pathway may become a therapeutic target for ischemic cerebrovascular disease in the future. |
