Objective To explore the neuroprotective effect and potential mechanism of Hirsu-tine in rat cerebral ischemia-reperfusion injury(CIRI).Methods SD rats were used to establish a mid-dle cerebral artery occlusion reperfusion(MCAO/R)model and were divided into 6 groups(n=6):Con-trol group;Model group;Hirsutine low-dose(5 mg/kg)group;Hirsutine medium dose(10 mg/kg)group;Hirsutine high-dose(20 mg/kg)group;Edaravone(30 mg/kg,positive control)group.TTC staining was performed on brain tissue,the cerebral infarction and neurobehavipral defects were meas-ured HE and Nissl staining were used to detect neuronal damage.Tunel staining was used to detect hipp-ocampal cell apoptosis;ELISA method was used to detect the levels of reactive oxygen species(ROS),malondialdehyde(MDA),superoxide dismutase(SOD),and glutathione peroxidase(GSH Px)in brain tissues.Western blotting is used to detect the expression level of proteins related to the mechanism.Re-sults The results showed that Hirsutine treatment significantly reduced cerebral infarction and neuronal damage in MCAO/R rats,and improved brain neurobehavioral deficits.Hirsutine effectively inhibited oxi-dative stress and cell apoptosis.In addition,Hirsutine activated the PI3K/Akt/Nrf2 pathway in MCAO/R rat neurons.Conclusion Hirsutine improveed oxidative stress and apoptosis in MCAO/R rat brain by activating PI3K/Akt/Nrf2 signaling pathway,thereby alleviating CIRI-induced neuronal injury.
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