人参皂甙Rbl对阿霉素所致慢性心力衰竭大鼠心肌细胞肿瘤坏死因子的影响（英文）

Influence of Ginsenoside-Rbl on cardiomyocyte tumor necrosis factor level in rats with adriamycin-induced chronic heart failure

目的:探讨人参皂甙Rbl(Gs-Rb1)减轻阿霉素所致的慢性心力衰竭(CHF)效应是否与改善肿瘤坏死因子受体(TNFR)及其配体:肿瘤坏死因子-α(TNF-α)水平有关。方法:阿霉素诱导的CHF大鼠模型被随机分为阿霉素组(n=15,接受阿霉素1μmol/L)和Gs-Rbl组(n=17,在阿霉素组的基础上接受Gs-Rbl 70mg·k-1g·d-1,),另正常Wistar大鼠被设为正常对照组(n=10)同时培养的乳鼠心肌细胞亦相应地分为正常对照组、阿霉素组和Gs-Rbl组。干预完毕后,检测并比较三组心脏超声、TNFR/TNF-α蛋白和mRNA水平。结果:1.体内:阿霉素组和Gs-Rbl组的TNFR-1[蛋白(0.67±0.04)kDa,(0.51±0.04)kDa;mRNA(0.81±0.03)bp,(0.49±0.05)bp],TNFR-2[蛋白(0.61±0.05)kDa,(0.47±0.03)kDa,mRNA(0.28±0.03)bp,(0.18±0.04)bp]]及TNF-α[蛋白TNF-α[protein(0.28±0.04)kDa,(0.20±0.03)kDa,mRNA(0.67±0.05)bp,(0.45±0.04)bp]水平显著高于正常对照组TNFR-1[蛋白(0.13±0.02)kDa,mRNA(0.19±0.05)bp],TNFR-2[蛋白(0.24±0.01)kDa,mRNA(0.13±0.02)bp],及TNF-α[蛋白(0.11±0.01)kDa,mRNA(0.26±0.05)bp](P<0.05或<0.01),且Gs-Rbl组的TNFR-1,TNFR-2及TNF-α蛋白和mRNA水平显著低于阿霉素组(P<0.05或<0.01);体外测定的各组结果相似,也是阿霉素组和Gs-Rbl组显著高于正常对照组(P<0.05或<0.01),Gs-Rbl组显著低于阿霉素组(P<0.05或<0.01)。结论:在阿霉素促发CHF进程中,TNFR/TNF-α的表达可能起着一定作用;人参皂甙Rbl改善阿霉素CHF效应可能与调整TNFR/TNF-α有关。

Objective：To explore whether relieving effect of Ginsenosides-Rb1 （Gs-Rb1 ） on chronic heart failure （CHF） induced by adriamycin is related to improving levels of tumor necrosis factor （TNF） receptor （TNFR） and ligand TNF-αor not .Methods：Adriamycin-induced CHF model rats were randomly divided into adriamycin group （n=15 ,received adriamycin 1 μmol/L） and Gs-Rb1 group （n=17 ,received Gs-Rb1 70 mg·k^-1g·d^-1 based on adriamycin group） ,another 10 healthy Wistar rats were selected as normal control group .Meanwhile ,cultured car-diomyocytes of neonatal rats were accordingly divided into normal control group ,adriamycin group and adriamycin＋Gs-Rb1 group .After intervention ,echocardiography ,levels of TNFR/TNF-αmRNA and protein were measured and compared among three groups .Results：（1） In vivo：Compared with normal control group TNFR-1 [protein （0.13 ± 0.02） kDa ,mRNA （0.19 ± 0.05） bp] , TNFR-2 [protein （0.24 ± 0.01） kDa ,mRNA （0.13 ± 0.02） bp] ,and TNF-α [protein （0.11 ± 0.01） kDa ,mRNA （0.26 ± 0.05） bp] ,the levels of TNFR-1 [protein （0.67 ± 0.04） kDa , （0.51 ± 0.04） kDa;mRNA （0.81 ± 0.03） bp , （0.49 ± 0.05） bp] , TNFR-2 [protein （0.61 ± 0.05） kDa ,（0.47 ± 0.03） kDa , mRNA （0.28 ± 0.03） bp , （0.18 ± 0.04） bp] and TNF-α [protein （0.28 ± 0.04） kDa ,（0.20 ± 0.03） kDa ,mRNA （0.67 ± 0.05） bp , （0.45 ± 0.04） bp] significantly rose （P〈0.05 or 〈0.01） in adriamycin group and Gs-Rb1 group;and those levels of TNFR-1 ,TNFR-2 , TNF-αprotein and mRNA of Gs-Rbl group were significant reduction than those of adriamycin group ; （2） In vitro：The results were similar , those of adriamycin group and Gs-Rb1 group were also significant rise than those of normal control group （ P〈0. 05 or 〈0. 01 ） , those of Gs-Rbl group were significant reduction than those of adriamycin group （ P〈 0. 05 or 〈0.01） .Conclusion：TNFR/TNF-αexpression may play a certain role in the process of adriamycin-induced CHF ;im-proving effect of Gs-Rb1 on adriamycin-induced CHF may be related to regulation of TNFR/TNF-α.