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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 investigate whether Gs-Rb1 attenuates the effects of doxorubicin-induced chronic heart failure (CHF) on TNF-α and tumor necrosis factor-α (TNF-α) ) Level related. Methods: Adriamycin-induced CHF rat models were randomly divided into doxorubicin group (n = 15, doxorubicin 1 μmol / L) and Gs-Rbl group (n = 17) (Gs-Rb1 70mg · k-1g · d-1, respectively). The normal Wistar rats (n = 10) were also divided into normal control group, Prime group and Gs-Rbl group. After intervention, three groups of heart ultrasound, TNFR / TNF-α protein and mRNA levels were detected and compared. TNFR-1 [(0.67 ± 0.04) kDa, (0.51 ± 0.04) kDa, (0.81 ± 0.03) kDa, (0.49 ± 0.05) bp] in mRNA and protein levels of adriamycin and Gs- (0.28 ± 0.03) kDa, (0.28 ± 0.03) bp, (0.18 ± 0.04) bp] and TNF-α [protein (0.13 ± 0.02) kDa, mRNA (0.19 ± 0.05) kDa, (0.20 ± 0.03) kDa, (0.67 ± 0.05) bp and (0.45 ± 0.04) bp were significantly higher than those in the normal control group (P <0.05), TNF-α [protein (0.11 ± 0.01) kDa, mRNA (0.26 ± 0.05) bp] Or <0.01). The mRNA and protein levels of TNFR-1, TNFR-2 and TNF-α in Gs-Rbl group were significantly lower than those in doxorubicin group (P <0.05 or <0.01) It was also significantly higher in the adriamycin-treated and Gs-Rbl-treated groups than in the normal control (P <0.05 or <0.01) and in the Gs-Rbl-treated group (P <0.05 or <0.01). CONCLUSION: The expression of TNFR / TNF-α may play a role in the process of adriamycin-induced CHF. The effect of ginsenoside Rbl on the improvement of doxorubicin-CHF may be related to the regulation of TNFR / TNF-α.