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作 者:朱琳[1] 王彦军[1] 俞天虹[1] 罗光华[1] 魏江[1] 于洋[1] 贾方[1] 孙建辉[1]
机构地区:[1]苏州大学附属第三医院心内科,江苏省常州市213003
出 处:《中国动脉硬化杂志》2015年第1期5-10,共6页Chinese Journal of Arteriosclerosis
基 金:国家自然科学基金资助(81300220)
摘 要:目的研究红景天苷对高同型半胱氨酸诱导的内皮细胞损伤的保护作用及其机制。方法不同浓度同型半胱氨酸(Hcy)预处理人脐静脉内皮细胞(HUVEC),再使用1 mmol/L Hcy与不同浓度红景天苷共同作用HUVEC。24 h后,MTT法检测细胞存活率。实时荧光定量PCR(RT-PCR)检测免疫球蛋白重链结合蛋白(Bip)和C/EBP同源蛋白(CHOP)的基因表达水平,Western blot检测Bip、CHOP蛋白表达水平、PKR内质网激酶(PERK)及内质网核信号转导蛋白1α(IRE1α)磷酸化水平。结果与正常对照组比较,Hcy组细胞存活率降低,Bip和CHOP的基因和蛋白水平升高,PERK和IRE1α的磷酸化水平升高(P<0.05)。与Hcy组比较,高浓度红景天苷(300μmol/L)与Hcy共同作用后细胞存活率升高,Bip和CHOP的基因和蛋白表达水平下降,PERK和IRE1α的磷酸化水平下降(P<0.05)。结论红景天苷对高同型半胱氨酸诱导的HUVEC损伤具有保护作用,其机制可能与抑制内质网应激信号通路的活化有关。Aim To discuss the protective effect and mechanism of salidroside on homocysteine( Hcy)-induced endothelial cell injury. Methods Human umbilical vein endothelial cells( HUVEC) were cultured in different concentrations of Hcy,then the concentration of positive significance( 1 mmol / L) was picked out. HUVEC were cultured with different concentrations of salidroside and Hcy concetration for 24 hours was chosen. Cell viability was assessed with MTT assay,the mRNA levels of Bip,CHOP were detected by real-time quantitative PCR( RT-PCR). The protein levels of Bip,CHOP,phosphorylation of PERK,IRE1α were examined by Western blot. Results We observed that Hcy( 0. 5 mmol/L,1 mmol/L,2 mmol/L and 4 mmol/L) induced dysfunction of HUVEC,increased the mRNA and protein levels of Bip and CHOP( P < 0. 05),and elevated PERK and IRE1α phosphorylation( P < 0. 05) in HUVEC. Salidroside attenuated the cell damage effects of Hcy on HUVEC in a dose-dependent manner. The cell viability of HUVEC were up-regulated by salidroside compared with Hcy treated group( P < 0. 05). We also found that mRNA and protein levels of Bip and CHOP were down-regulated by salidroside( 300 μmol / L) compared with Hcy treated group( P < 0. 05),while PERK and IRE1α phosphorylation were increased( P < 0. 05) in HUVEC. Conclusions These findings suggested that salidroside could attenuate high Hcy induced injury in HUVEC,partly through inhibiting endoplasmic reticulum stress pathway.
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