Cyclovirobuxinum D Alleviates Cardiac Hypertrophy in Hyperthyroid Rats by Preventing Apoptosis of Cardiac Cells and Inhibiting the p38 Mitogen-Activated Protein Kinase Signaling Pathway

Objective： To investigate the underlying mechanisms of cyclovirobuxinum D（Cvb-D） on alleviating cardiac hypertrophy in rats. Methods： Sprague-Dawley rats were randomly divided into 5 groups： control group; levothyroxine-induced cardiac hypertrophy group（model）; levothyroxine-induced cardiac hypertro...

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Bibliographic Details
Published in:Chinese journal of integrative medicine 2017-10, Vol.23 (10), p.770-778
Main Authors: Wu, Jun-biao, Zhou, Yuan, Liang, Chun-ling, Zhang, Xiao-jun, Lai, Jie-mei, Ye, Shu-fang, Ouyang, Hui, Lin, Jin, Zhou, Jiu-yao
Format: Article
Language:English
Subjects:
Animals
Apoptosis - drug effects
Cardiomegaly - complications
Cardiomegaly - drug therapy
Cardiomegaly - enzymology
Cardiomegaly - pathology
Drugs, Chinese Herbal - chemistry
Drugs, Chinese Herbal - pharmacology
Drugs, Chinese Herbal - therapeutic use
Fatty Acids - metabolism
Hemodynamics - drug effects
Hyperthyroidism - complications
Hyperthyroidism - drug therapy
Hyperthyroidism - enzymology
Hyperthyroidism - pathology
Hypertrophy, Left Ventricular - complications
Hypertrophy, Left Ventricular - drug therapy
Hypertrophy, Left Ventricular - pathology
Kidney - drug effects
Kidney - pathology
Malondialdehyde - metabolism
MAP Kinase Signaling System - drug effects
MAPK信号通路
Medicine
Medicine & Public Health
mRNA表达
Myocytes, Cardiac - drug effects
Myocytes, Cardiac - pathology
Original Article
p38 Mitogen-Activated Protein Kinases - metabolism
p38丝裂原活化蛋白激酶
Phosphorylation - drug effects
Rats, Sprague-Dawley
RNA, Messenger - genetics
RNA, Messenger - metabolism
Superoxide Dismutase - metabolism
大鼠
心肌细胞凋亡
心肌肥大
预防
黄杨
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Summary:Objective： To investigate the underlying mechanisms of cyclovirobuxinum D（Cvb-D） on alleviating cardiac hypertrophy in rats. Methods： Sprague-Dawley rats were randomly divided into 5 groups： control group; levothyroxine-induced cardiac hypertrophy group（model）; levothyroxine-induced cardiac hypertrophy ＋ Cvb-D group（Cvb-D）; levothyroxine-induced cardiac hypertrophy ＋ captopril group（captopril）; levothyroxine-induced cardiac hypertrophy ＋ SB203580 group（SB203580）, n=10 for each group. Rats were daily administered the respective drugs continuously for14 days by gastric gavage. A rat model of cardiac hypertrophy was established by intraperitoneal injection of levothyroxine to investigate whether Cvb-D protects against cardiac hypertrophy by inhibiting the p38 mitogen-activated protein kinase（MAPK） signaling pathway and preventing apoptosis of cardiac cells. Results： Treatment with Cvb-D significantly deceased left ventricle hypertrophy, improved the histopathology, hemodynamic conditions, and cardiac function in rats with cardiac hypertrophy. Compared with the normal control group, in rats with cardiac hypertrophy, expression of bax in the heart and phospho-p38 MAPK protein levels were significantly up-regulated（P〈0.01 or 0.05）, whereas the bcl-2 protein level was downregulated（P〈0.01）. In contrast, Cvb-D treatment reversed the changes in bax and phospho-p38 MAPK protein levels but increased the bcl-2 protein level（P〈0.01 or 0.05）, and these effects were similar to those of captopril and SB203580（a specific p38 MAPK inhibitor） treatment. Furthermore, both Cvb-D, captopril and SB203580 reduced m RNA expression of p38α, p38β, c-fos, and c-jun m RNA, and Cvb-D had a stronger effect（P〈0.01）. Conclusion： These results demonstrate that Cvb-D protects against cardiac hypertrophy, which is possibly mediated by prevention of cardiac cell apoptosis and inhibition of the p38 MAPK signaling pathway.
ISSN:1672-0415
1993-0402
DOI:10.1007/s11655-015-2299-7