γ-linolenic Acid Improves Cognitive Impairment in Mice with Cerebral Infarction by Down-Regulating Oxidative Stress Response and Inhibiting NLRP3-Mediated Pyroptosis
Objective:To investigate the effect and mechanism of γ-linolenic acid(GLA)on cognitive impairment in mice with cerebral ischemia.Methods:Eighteen male mice were randomly divided into three groups:control group(n=6),model group(n=6),and GLA group(n=6).The cerebral infarction model was established in the model group and GLA group by middle cerebral artery occlusion(MCAO),and sham surgery was performed in the control group.Mice in the control and model groups were administered saline(1 mg/kg)by gavage daily,while mice in the GLA group were administered GLA(1 mg/kg)by gavage daily for 14 days.Morris water maze test was used to evaluate the cognitive impairment of mice.The infarct area and neuronal apoptosis in the brain tissues were measurd by HE staining and TUNEL staining,respectively.The expression levels of P22,P47,NLRP3,IL-1β,GSDMD,and Caspase-1 proteins in the hippocampus of mice were detected by Western blot.Results:The escape latency and crossing number of mice in the model group were shorter and more than those in the GLA group and control group,respectively.The infarct area and the number of apoptotic neurons in the brain tissues of the model group were the largest,followed by the GLA group,and there was no cerebral infarction or neuronal apoptosis in the control group.The expression levels of P22,P47,NLRP3,IL-1β,GSDMD,and Caspase-1 proteins in the model group were higher than those in the GLA group and control group,while those in the GLA group were higher than those in the control group.Conclusion:GLA improves cognitive impairment in mice with cerebral ischemia by down-regulating oxidative stress and inhibiting NLRP3-mediated pyroptosis.
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