OBJECTIVE Oleoylethanolamide(OEA) is an endogenous peroxisome proliferatoractivated receptor alpha(PPARα) agonist that acts on the peripheral control of energy metabolism.Previous studies have shown that OEA exerts n...OBJECTIVE Oleoylethanolamide(OEA) is an endogenous peroxisome proliferatoractivated receptor alpha(PPARα) agonist that acts on the peripheral control of energy metabolism.Previous studies have shown that OEA exerts neuroprotection after cerebral ischemia.However,whether OEA affects the outcomes of diabetes-induced encephalopathy(DE) requires further study.METHODS The chronic effects of OEA on DE were evaluated in C57BL/6 and PPARαknockout mice,individually.The cognitive function was assessed with Morris water maze.The expression of receptor for advanced glycation end products(RAGE) and phosphorylation of Tau in mice hippocampus were determined using Western blotting.The influence of OEA in neuron loss and neuroplasticity were assessed with immunofluorescent staining and Western blotting.RESULTS OEA markedly ameliorated performance in the Morris water maze,which was correlated with its capabilities of suppressing glycometabolism and phosphorylation of Tau in the hippocampus.OEA offered protection from diabetes-induced impairments in hippocampal neuroplasticity.Furthermore,the changes in Morris water maze performance and neuron loss could not be observed in PPARα knockout mouse models with OEA administration.CONCLUSION The ability of OEA to control PPARα signaling can serve as a novel neuroprotective approach for the treatment of diabetes-induced encephalopathy.展开更多
目的:观察隔药饼灸对动脉粥样硬化(artherosc lerosis,AS)兔主动脉内皮细胞过氧化酶体增殖物激活型受体γ(Peroxisom e proliferator-activated receptor,γPPARγ)的影响,探讨隔药饼灸延迟AS形成的作用机理。方法:将75只新西兰大耳白兔...目的:观察隔药饼灸对动脉粥样硬化(artherosc lerosis,AS)兔主动脉内皮细胞过氧化酶体增殖物激活型受体γ(Peroxisom e proliferator-activated receptor,γPPARγ)的影响,探讨隔药饼灸延迟AS形成的作用机理。方法:将75只新西兰大耳白兔,通过高脂饲料喂养及免疫损伤法建立兔AS模型。然后随机分为5组,每组15只,即:空白组(空白对照组);模型组(AS模型组);直接灸组(AS模型+艾炷直接灸);隔药饼灸组(AS模型+隔药饼灸);西药组(AS模型+阿托伐他汀)。采用逆转录聚合酶链反应(RT-PCR)检测兔主动脉内皮细胞PPARγ蛋白表达。结果:模型组主动脉内皮细胞PPARγ的蛋白表达明显低于空白组、西药组、隔药饼灸和直接灸组,且有显著性差异(P<0.01,P<0.05);西药组与直接灸组比较有显著性差异(P<0.05)。结论:西药组、隔药饼灸和直接灸组均能通过激活动脉粥样硬化兔主动脉内皮细胞PPARγ的蛋白表达,起到延迟动脉粥样硬化斑块形成的作用,西药组与隔药饼灸组作用相当,而西药组的作用要强于直接灸组。展开更多
基金Fun-damental Research Funds for the Central Universities (20720180042)Health Science ResearchPersonnel Training Program of Fujian Province(2018-CXB-30)+2 种基金Natural Science Foundation of Fujian, China (2016J014152016D024)Science and Technology Project of Xi
文摘OBJECTIVE Oleoylethanolamide(OEA) is an endogenous peroxisome proliferatoractivated receptor alpha(PPARα) agonist that acts on the peripheral control of energy metabolism.Previous studies have shown that OEA exerts neuroprotection after cerebral ischemia.However,whether OEA affects the outcomes of diabetes-induced encephalopathy(DE) requires further study.METHODS The chronic effects of OEA on DE were evaluated in C57BL/6 and PPARαknockout mice,individually.The cognitive function was assessed with Morris water maze.The expression of receptor for advanced glycation end products(RAGE) and phosphorylation of Tau in mice hippocampus were determined using Western blotting.The influence of OEA in neuron loss and neuroplasticity were assessed with immunofluorescent staining and Western blotting.RESULTS OEA markedly ameliorated performance in the Morris water maze,which was correlated with its capabilities of suppressing glycometabolism and phosphorylation of Tau in the hippocampus.OEA offered protection from diabetes-induced impairments in hippocampal neuroplasticity.Furthermore,the changes in Morris water maze performance and neuron loss could not be observed in PPARα knockout mouse models with OEA administration.CONCLUSION The ability of OEA to control PPARα signaling can serve as a novel neuroprotective approach for the treatment of diabetes-induced encephalopathy.
文摘目的:观察隔药饼灸对动脉粥样硬化(artherosc lerosis,AS)兔主动脉内皮细胞过氧化酶体增殖物激活型受体γ(Peroxisom e proliferator-activated receptor,γPPARγ)的影响,探讨隔药饼灸延迟AS形成的作用机理。方法:将75只新西兰大耳白兔,通过高脂饲料喂养及免疫损伤法建立兔AS模型。然后随机分为5组,每组15只,即:空白组(空白对照组);模型组(AS模型组);直接灸组(AS模型+艾炷直接灸);隔药饼灸组(AS模型+隔药饼灸);西药组(AS模型+阿托伐他汀)。采用逆转录聚合酶链反应(RT-PCR)检测兔主动脉内皮细胞PPARγ蛋白表达。结果:模型组主动脉内皮细胞PPARγ的蛋白表达明显低于空白组、西药组、隔药饼灸和直接灸组,且有显著性差异(P<0.01,P<0.05);西药组与直接灸组比较有显著性差异(P<0.05)。结论:西药组、隔药饼灸和直接灸组均能通过激活动脉粥样硬化兔主动脉内皮细胞PPARγ的蛋白表达,起到延迟动脉粥样硬化斑块形成的作用,西药组与隔药饼灸组作用相当,而西药组的作用要强于直接灸组。
