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Pharmacological effects and mechanisms of andrographolide on isoproterenol induced heart failure in mice |
Hits 1565 Download times 1229 Received:January 02, 2018 |
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DOI
10.11656/j.issn.1673-9043.2018.03.12 |
Key Words
Andrographolide;heart failure;network pharmacology;mechanism |
Author Name | Affiliation | E-mail | ZHANG Huimin | School of Chinese Medicine, Beijing University of Traditional Chinese Medicine, Beijing 100029, China | | REN Yinglu | School of Chinese Medicine, Beijing University of Traditional Chinese Medicine, Beijing 100029, China | | LIU Jinying | School of Chinese Medicine, Beijing University of Traditional Chinese Medicine, Beijing 100029, China | | XIE Xuan | School of Chinese Medicine, Beijing University of Traditional Chinese Medicine, Beijing 100029, China | | WANG Qing | School of Chinese Medicine, Beijing University of Traditional Chinese Medicine, Beijing 100029, China | | SU Congping | School of Chinese Medicine, Beijing University of Traditional Chinese Medicine, Beijing 100029, China | | WANG Wei | School of Chinese Medicine, Beijing University of Traditional Chinese Medicine, Beijing 100029, China | | GUO Shuzhen | School of Chinese Medicine, Beijing University of Traditional Chinese Medicine, Beijing 100029, China | guoshz@bucm.edu.cn |
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Abstract
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[Objective] To study on the efficacy of andrographolide on heart failure induced by isoproterenol (ISO) in mice, and investigated its mechanism by combing experimental validation with network pharmacological prediction.[Methods] Mice with heart failure, induced by ISO, were randomly divided into control group, model group, andrographolide group and digoxin group. The cardiac function of mice was analyzed by echocardiography, morphology and pathology. The target was predicted by bioinformatics analysis tool (BATMAN-TCM), and the mRNA level of potential target gene was detected by real-time fluorescence quantitative PCR.[Results] Compared with the control group, EF, FS and E/A were significantly decreased in model group (P<0.05), LVIDs was significantly increased (P<0.05), cardiomyocyte hypertrophy, accompanied by sinus dilatation and connective tissue hyperplasia was observed, and the expression of HMGCR gene in myocardium was upregulated (P<0.05). Compared with the model group, the EF, FS and E/A was improved by andrographolide significantly (P<0.05), LVIDs was significantly decreased (P<0.01), the cardiomyocyte hypertrophy was alleviated, and the expression of HMGCR gene in myocardium was significantly downregulated (P<0.05).[Conclusion] Andrographolide can improve heart function of mice with heart failure induced by isoprenaline, and its mechanism may be related to the inhibition of HMG-CoA reductase and regulation of cholesterol synthesis. |
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