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作 者:周宇 李晶[2] 鲍翠玉[2] ZHOU Yu;LI Jing;BAO Cui-yu(College of Pharmacy,Hubei University of Science and Technology,Xianning Hubei 437100,China;Hubei Province Key Lab on Cardiovascular,Cerebrovascular and Metabolic Disorders, Hubei University of Science and Technology,Xianning Hubei 437100,China)
机构地区:[1]湖北科技学院药学院,湖北咸宁437100 [2]湖北科技学院糖尿病心脑血管病变湖北省重点实验室,湖北咸宁437100
出 处:《中国药理学通报》2018年第9期1283-1288,共6页Chinese Pharmacological Bulletin
基 金:国家自然科学基金资助项目(No 51703055);湖北省自然科学基金资助项目(No 2017CFB99;2015CFC773);湖北省教育厅科学研究计划项目(No B201696);湖北科技学院糖尿病专项基金(No 2016-18XZ09;14ZX-02)
摘 要:目的探讨姜黄素纳米粒(curcumin nanoparticles,CurNPs)对高脂诱导的心肌细胞损伤的保护作用。方法采用棕榈酸(palmitic acid,PA)刺激H9c2心肌细胞,建立心肌细胞脂毒性损伤模型,Cur-NPs预处理,MTT法检测细胞增殖情况;活性氧(reactive oxygen species,ROS)试剂盒检测细胞内ROS水平;TUNEL试剂盒检测细胞凋亡情况;免疫印迹法检测细胞内质网应激和凋亡信号通路相关蛋白的表达水平。结果高脂可引起细胞增殖率的降低,ROS水平明显升高,细胞形态出现明显的病理性损伤改变,凋亡细胞明显增多;GRP78、CHOP和caspase-3表达水平明显增加,Bax/Bcl-2的比值升高。姜黄素纳米粒可以逆转上述变化。结论姜黄素纳米粒能够明显降低高脂诱发的心肌细胞ROS的产生,降低心肌细胞内质网应激和凋亡相关蛋白的表达,从而抑制高脂所致的H9c2心肌细胞损伤。To investigate the protective effect of curcumin nanoparticles(Cur-NPs)against high-fat-induced cardiomyocyte injury.Methods H9c2 cardiomyocytes were stimulated with palmitic acid(PA)to establish a rat model of lipotoxicity injury.The Cur-NPs were pretreated.MTT assay was used to detect cell proliferation.The reactive oxygen species(ROS)kit was used to detect intracellular reactive oxygen species and the cells were detected with the TUNEL kit.Apoptosis was detected by Western blot,and the expression levesl of endoplasmic reticulum stress and apoptotic signaling pathway related proteins were determined.Results High fat might cause the decrease of cell proliferation rate.The level of ROS obviously increased,and the pathological changes of cell morphology were evident.Apoptosis was obviously aggravated.The expression of GRP78,CHOP and caspase-3 apparently increased,and the Bax/Bcl-2 ratio elevated,which could all be reversed by Cur-NPs.Conclusions Cur-NPs significantly reduces the production of ROS induced by hyperlipidemia and reduces the expression of endoplasmic reticulum stress and apoptosis-related proteins in cardiomyocytes,thereby inhibiting the damage of H9c2 cardiomyocytes induced by high fat.
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