| Objective: To observe the effects of Compound C, an AMPK inhibition, on themorphology and function of astrocytes after cerebral ischemia/reperfusion injury in mice,to explore the neuroprotection mechanism of inhibiting AMPK activity. Methods:72maleKunming mice were randomly divided into sham group, saline group and drug-treatedgroup (24mice for each group). Establish the transient middle cerebral artery occlusion(MCAO) models. Each mouse in drug-treated group was given an intraperitoneal inject ofCompound C (20mg/kg) after occlusion, each mouse in saline group was administered theequal saline in stead of drug, and nothing was injected in sham group. Afterischemia/reperfusion for24h, the neurologic impairment scores was tested by LongaScore method, the Infarct volume was observed by TTC staining, the pathology varietywas observed by HE staining, the expression of astrocyte-specific GFAP was detectedby immunohistochemistry, and the mRNA expression connexin43and EAAT2wasdetected by RT-PCR. Result: After cerebral ischemia/reperfusion for24h,(1) comparedwith the saline group, infarct volume and the neurological function score were bothdecreased significantly in the drug-treated group (P<0.01, P<0.05, respectively);(2)compared with the saline group, GFAP-labeled cells were decreased significantly in thedrug-treated group (P<0.05);(3) the drug-treated group could up-regulate the expressionof Cx43mRNA in infarct side (P<0.05);(4) compared with the sham group, both thesaline group and drug-treated group could up-regulate the expression of EAAT mRNA ininfarct side (P<0.05); The drug-treated group showed an upward trend of EAAT2expression level with the saline group, but these differences were not statisticallysignificant（P=0.235）. Conclusion: Compound C could have neuroprotection effects incerebral ischemia/reperfusion mice by inhibition AMPK activity. Its mechanism may berelated to inhibit excessive astrocytes activation, increase of Cx43and EAAT2expression. |
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