| Objective:To investigate the protection mechanism of acupuncture on transient MCAO rat mode through the effects of the acupuncture on related genes expression in PERK pathway were detected,Then the mechanism of neuroprotective effect produced by acupuncture were eluciateded, which provide us with new theory for clinical treatment of cerebral ischemia.Methods:To establish an middle cerebral artery oeclusion(MCAO) mode in rats. The rats were randomly divided into sham-operation group, normal group, MCAO mode group,acupuncture group, annaoping-chong pill group,with12rats in each group。To observing the scores of the neurologic impairment, to surveying eares of cerebral infarction by TTC staining and the expression of p-PERKã€eIF2αã€ATF4mRNA were measured with Methods of reverse transcription-polymerase chain reaction (RT-PCR).Results:1. Compared to the others, the scores of the neurologic impairment and the eares of cerebral infarction were significant differences (P<0.01).Compared to the MCAO mdel, the scores of the neurologic impairment and the eares of cerebral infarction were reduced accordingly in acupuncture group and Annaopingchong pill group (P<0.05).the acupuncture group Comparing the Annaopingchong pill group, the scores of the neurologic impairment and the eares of cerebral infarction were not statistically significant(P>0.05).2. The expression of PERKã€eIF2aã€ATF4were up-regulated in peri-infarction after cerebral ischemia/reperfusion in Rats (P<0.01). the expression level of PERKã€eIF2αã€ATF4mRNA in intervention models were reduced accordingly (P<0.01). the acupuncture group Comparing the Annaopingchong pill group, the expression level of PERKã€eIF2α ATF4mRNA were not statistically significant (P>0.05).Conclusion:1.Acupuncture could reduce neurological deficits and cerebral infarction volume after cerebral ischemia/reperfusion in rats.2. Acupuncture could inhibit endoplasmic reticulum stress reaction and apoptosis signal pathway by the expressive down-regulation of PERK,ATF4,and eIF2a after cerebral ischemia/reperfusion in rats, which may result in decreases of neuronal apoptosis and ischemical reperfusion injury. |