河北医药
河北醫藥
하북의약
Hebei Medical Journal
2015年
22期
3365-3368
,共4页
徐涛%张哲%王锦鹏%田丰永%刘欣
徐濤%張哲%王錦鵬%田豐永%劉訢
서도%장철%왕금붕%전봉영%류흔
丹参酮ⅡA磺酸钠%阿托伐他汀%冠心病%Toll样受体4%免疫功能
丹參酮ⅡA磺痠鈉%阿託伐他汀%冠心病%Toll樣受體4%免疫功能
단삼동ⅡA광산납%아탁벌타정%관심병%Toll양수체4%면역공능
sodium tanshinoneⅡA sulfonate%atorvastatin%coronary artery diseases%TLR4%immune function
目的:观察丹参酮ⅡA磺酸钠联合阿托伐他汀对冠心病患者TLR4炎症信号通路及免疫相关指标的影响,以TLR4炎症信号通路为靶点探讨丹参酮ⅡA磺酸钠治疗冠心病的可能机制。方法选取2014年1月至2015年1月诊治的冠心病患者160例,随机分为对照组和观察组,每组80例。对照组在常规治疗基础上给予阿托伐他汀治疗,观察组在对照组基础上加用丹参酮ⅡA磺酸钠注射液,疗程为30 d。采用Real time-PCR测定外周血单个核细胞TLR4 mRNA表达。采用酶联免疫吸附实验(ELISA)测定血清白介素-6(IL-6)、超敏C反应蛋白(hs-CRP)、肿瘤坏死因子-α( TNF-α)、基质金属白酶-9( MMP-9)及抗氧化修饰低密度脂蛋白( ox-LDL)抗体水平。流式细胞仪测定外周血淋巴细胞亚群指标(CD3+、CD4+、CD8+、CD4+/CD8+)变化。免疫比浊法测定免疫球蛋白(IgA、IgG、IgM)及补体C3、C4水平。结果与治疗前比较,治疗后2组TLR4 mRNA、IL-6、hs-CRP、TNF-α、MMP-9、ox-LDL、IgA、IgG、IgM、C3、C4水平显著降低( P <0怂.05),CD3+、CD4+、CD8+、CD4+/CD8+水平显著升高( P <0.05),但观察组上述指标改善程度优于对照组( P <0.05)。结论丹参酮ⅡA磺酸钠联合阿托伐他汀能抑制外周血TLR4 mRNA炎症信号通路的激活,并改善机体免疫功能紊乱,这可能是丹参酮ⅡA磺酸钠发挥治疗作用的机制之一。
目的:觀察丹參酮ⅡA磺痠鈉聯閤阿託伐他汀對冠心病患者TLR4炎癥信號通路及免疫相關指標的影響,以TLR4炎癥信號通路為靶點探討丹參酮ⅡA磺痠鈉治療冠心病的可能機製。方法選取2014年1月至2015年1月診治的冠心病患者160例,隨機分為對照組和觀察組,每組80例。對照組在常規治療基礎上給予阿託伐他汀治療,觀察組在對照組基礎上加用丹參酮ⅡA磺痠鈉註射液,療程為30 d。採用Real time-PCR測定外週血單箇覈細胞TLR4 mRNA錶達。採用酶聯免疫吸附實驗(ELISA)測定血清白介素-6(IL-6)、超敏C反應蛋白(hs-CRP)、腫瘤壞死因子-α( TNF-α)、基質金屬白酶-9( MMP-9)及抗氧化脩飾低密度脂蛋白( ox-LDL)抗體水平。流式細胞儀測定外週血淋巴細胞亞群指標(CD3+、CD4+、CD8+、CD4+/CD8+)變化。免疫比濁法測定免疫毬蛋白(IgA、IgG、IgM)及補體C3、C4水平。結果與治療前比較,治療後2組TLR4 mRNA、IL-6、hs-CRP、TNF-α、MMP-9、ox-LDL、IgA、IgG、IgM、C3、C4水平顯著降低( P <0慫.05),CD3+、CD4+、CD8+、CD4+/CD8+水平顯著升高( P <0.05),但觀察組上述指標改善程度優于對照組( P <0.05)。結論丹參酮ⅡA磺痠鈉聯閤阿託伐他汀能抑製外週血TLR4 mRNA炎癥信號通路的激活,併改善機體免疫功能紊亂,這可能是丹參酮ⅡA磺痠鈉髮揮治療作用的機製之一。
목적:관찰단삼동ⅡA광산납연합아탁벌타정대관심병환자TLR4염증신호통로급면역상관지표적영향,이TLR4염증신호통로위파점탐토단삼동ⅡA광산납치료관심병적가능궤제。방법선취2014년1월지2015년1월진치적관심병환자160례,수궤분위대조조화관찰조,매조80례。대조조재상규치료기출상급여아탁벌타정치료,관찰조재대조조기출상가용단삼동ⅡA광산납주사액,료정위30 d。채용Real time-PCR측정외주혈단개핵세포TLR4 mRNA표체。채용매련면역흡부실험(ELISA)측정혈청백개소-6(IL-6)、초민C반응단백(hs-CRP)、종류배사인자-α( TNF-α)、기질금속백매-9( MMP-9)급항양화수식저밀도지단백( ox-LDL)항체수평。류식세포의측정외주혈림파세포아군지표(CD3+、CD4+、CD8+、CD4+/CD8+)변화。면역비탁법측정면역구단백(IgA、IgG、IgM)급보체C3、C4수평。결과여치료전비교,치료후2조TLR4 mRNA、IL-6、hs-CRP、TNF-α、MMP-9、ox-LDL、IgA、IgG、IgM、C3、C4수평현저강저( P <0종.05),CD3+、CD4+、CD8+、CD4+/CD8+수평현저승고( P <0.05),단관찰조상술지표개선정도우우대조조( P <0.05)。결론단삼동ⅡA광산납연합아탁벌타정능억제외주혈TLR4 mRNA염증신호통로적격활,병개선궤체면역공능문란,저가능시단삼동ⅡA광산납발휘치료작용적궤제지일。
Objective To investigate the effect of sodium tanshinone ⅡA sulfonate combined with atorvastatin on TLR4 inflammatory signal pathway and immune function of patients with coronary heart diseases ( CHD) in order to explore the possible action mechanism of sodium tanshinone ⅡA sulfonate in treatment of CHD.Methods One hundred and sixty patients with coronary artery diseases who were admitted into our hospital from January 2014 to January 2015 were randomly divided into observation group ( n =80 ) and control group ( n =80 ) .The patients in control group were treated with atorvastatin,on the basis of symptomatic treatment,however, the other patients in observation group, on the basis of the control group, were treated with sodium tanshinoneⅡA sulfonate,with a treatment course of 30 days for both groups.The expression levels of TLR4 mRNA in peripheral blood were detected by Real time-PCR.The serum levels of IL-6, hs-CRP, TNF-α, MMP-9 and ox-LDL were measured by ELISA.The lymphocyte subsets ( CD3+,CD4+,CD8+, CD4+/CD8+) were detected by flow cytometry.The immunoglobulins( IgA, IgG, IgM) and complement levels ( C3, C4 ) were examined by turbidimetric inhibition immuno assay for both groups.Results As compared with those before treatment,the levels of TLR 4 mRNA,IL-6, hs-CRP,TNF-α,MMP-9,ox-LDL,IgA,IgG,IgM,C3,C4 were significantly decreased after treatment for both groups ( P <0.05),however, the levels of CD3+, CD4+, CD8+, CD4+/CD8+ were significantly increased ( P <0.05), moreover, the observation group was superior to control group in the improvement degree of these indexes ( P <0.05).Conclusion Sodium tanshinoneⅡA sulfonate combined with atorvastatin can significantly inhibit the activation of TLR4 inflammatory signal transduction pathway and can improve immunological function disorders,which may be one of the action mechanisms of sodium tanshinoneⅡA sulfonate in treatment of CHD.