中国社区医师
中國社區醫師
중국사구의사
Chinese Community Doctors
2014年
22期
7-8,14
,共3页
程莹%鲁永织%孙敏%张卓琦
程瑩%魯永織%孫敏%張卓琦
정형%로영직%손민%장탁기
阿托伐他汀%血管平滑肌细胞%肿瘤坏死因子%炎性反应
阿託伐他汀%血管平滑肌細胞%腫瘤壞死因子%炎性反應
아탁벌타정%혈관평활기세포%종류배사인자%염성반응
Atorvastatin%Vascular smooth muscle cell%Tumor necrosis factor%Inflammatory response
目的:探讨阿托伐他汀(Atv)在转录水平的抗炎作用机制。方法:将构建好的含有人类TNF-α启动子的以虫荧光素酶(Luciferase)为报告基因的质粒DNA转染至体外培养的平滑肌细胞中,以AngⅡ刺激并经不同浓度的Atv处理后,通过检测Luciferase的活性来观察启动子活性的变化。结果:启动子在VSMCs中可高效稳定的表达;而经AngⅡ刺激的VSMCs中,TNF-α启动子活性较未受刺激时明显上调(P<0.05)。在VSMCs中0.1~10μmol/L的Atv可抑制经AngⅡ刺激后上调表达的TNF-α启动子活性,并且呈现剂量依赖关系(P<0.05)。结论:Atv对TNF-α启动子活性的抑制,证明了其对促炎细胞因子在转录水平的潜在抑制作用。
目的:探討阿託伐他汀(Atv)在轉錄水平的抗炎作用機製。方法:將構建好的含有人類TNF-α啟動子的以蟲熒光素酶(Luciferase)為報告基因的質粒DNA轉染至體外培養的平滑肌細胞中,以AngⅡ刺激併經不同濃度的Atv處理後,通過檢測Luciferase的活性來觀察啟動子活性的變化。結果:啟動子在VSMCs中可高效穩定的錶達;而經AngⅡ刺激的VSMCs中,TNF-α啟動子活性較未受刺激時明顯上調(P<0.05)。在VSMCs中0.1~10μmol/L的Atv可抑製經AngⅡ刺激後上調錶達的TNF-α啟動子活性,併且呈現劑量依賴關繫(P<0.05)。結論:Atv對TNF-α啟動子活性的抑製,證明瞭其對促炎細胞因子在轉錄水平的潛在抑製作用。
목적:탐토아탁벌타정(Atv)재전록수평적항염작용궤제。방법:장구건호적함유인류TNF-α계동자적이충형광소매(Luciferase)위보고기인적질립DNA전염지체외배양적평활기세포중,이AngⅡ자격병경불동농도적Atv처리후,통과검측Luciferase적활성래관찰계동자활성적변화。결과:계동자재VSMCs중가고효은정적표체;이경AngⅡ자격적VSMCs중,TNF-α계동자활성교미수자격시명현상조(P<0.05)。재VSMCs중0.1~10μmol/L적Atv가억제경AngⅡ자격후상조표체적TNF-α계동자활성,병차정현제량의뢰관계(P<0.05)。결론:Atv대TNF-α계동자활성적억제,증명료기대촉염세포인자재전록수평적잠재억제작용。
Objective:To explore the anti-inflammatory action mechanism on transcriptional level of atorvastatin(Atv).Methods:The plasmid DNA had luciferase as the reporter gene and human TNF alpha promoter.The plasmid DNA was transfected to smooth muscle cell in vitro culture.It was stimulated by AngⅡand disposed by different concentrations of Atv.The change of the promoter activity was observed by detecting the activity of Luciferase.Results:The promoter could highly efficient and stable expression in VSMCs.While VSMCs was stimulated by AngⅡ,TNF-α promoter activity was obviously up-regulated than without stimulation(P<0.05).0.1~10 μ mol/L Atv could inhibit the higher expression of TNF-α promoter activity in VSMCs,and it was a dose-dependent manner(P<0.05).Conclusion:The inhibition of Atv on the TNF-α promoter activity proves its potential inhibition of proinflammatory cytokines at transcriptional level.