Influence of Ginsenoside-Rbl on cardiomyocyte tumor necrosis factor level in rats with adriamycin-induced chronic heart failure
10.3969/j.issn.1008-0074.2015.03
- VernacularTitle: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
- Author:
Hongliang KONG
;
Yujie WANG
- Publication Type:Journal Article
- Keywords:
Ginsenosides;
Heart failure;
Tumor Necrosis Factor-alpha;
Adriamycin
- From:
Chinese Journal of cardiovascular Rehabilitation Medicine
2015;24(3):283-288
- CountryChina
- Language:English
-
Abstract:
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-α or 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•kg-1•d-1 based on adriamycin group), another 10 healthy Wistar rats were selected as normal control group. Meanwhile, cultured cardiomyocytes of neonatal rats were accordingly divided into normal control group, adriamycin group and adriamycin+Gs-Rb1 group. After intervention, echocardiography, levels of TNFR/TNF-α mRNA 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]，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-α protein 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-α expression may play a certain role in the process of adriamycin-induced CHF; improving effect of Gs-Rb1 on adriamycin-induced CHF may be related to regulation of TNFR/TNF-α.
- Full text:P020151009583585518495.doc
