The protective effects of liguzinediol on congestive heart failure induced by myocardial infarction and its relative mechanism
Abstract Background Heart failure (HF) is one of the most common causes of cardiovascular diseases in the world. Currently, the drugs used to treat HF in the clinic may cause serious side effects. Liguzinediol, 2, 5-dimethyl-3, 6-dimethyl-pyrazine, is a compound synthesized after the structural modi...
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BMC
2020-06-01
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Online Access: | http://link.springer.com/article/10.1186/s13020-020-00345-7 |
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author | Qi Chen Dini Zhang Yunhui Bi Weiwei Zhang Yuhan Zhang Qinghai Meng Yu Li Huimin Bian |
author_facet | Qi Chen Dini Zhang Yunhui Bi Weiwei Zhang Yuhan Zhang Qinghai Meng Yu Li Huimin Bian |
author_sort | Qi Chen |
collection | DOAJ |
description | Abstract Background Heart failure (HF) is one of the most common causes of cardiovascular diseases in the world. Currently, the drugs used to treat HF in the clinic may cause serious side effects. Liguzinediol, 2, 5-dimethyl-3, 6-dimethyl-pyrazine, is a compound synthesized after the structural modification of ligustrazine (one active ingredient of Szechwan Lovage Rhizome). We aimed to observe the effects of liguzinediol on preventing HF and explore the related mechanisms. Methods The ligation of left anterior descending coronary artery was operated to established the myocardial infarction (MI) model in Sprague–Dawley rats. Cardiac functions were recorded by echocardiography and hemodynamics. The changes in the Renin–Angiotensin–Aldosterone System (RAAS), inflammation, and oxidative stress were detected by radioimmunoassay and Elisa kits. Western blot and real-time PCR were applied to determine the expressions of the TGF-β1/Smads pathway. Results Firstly, liguzinediol enhanced the systolic and diastolic functions of the heart in MI rats. Liguzinediol improved ventricular remodeling by reducing myocardial cell necrosis, as well as reducing collagen deposition and myocardial fibrosis. Then, liguzinediol suppressed the activation of RAAS, inhibited the synthesis of pro-inflammation factors, and reduced oxidative stress. In the end, liguzinediol also down-regulated the expressions of the TGF-β1/Smads pathway. Conclusions Liguzinediol could alleviate HF caused by MI in rats, and the protective effect was associated with the regulation of the TGF-β1/Smads pathway. |
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spelling | doaj.art-a6b4b2a731d04beeb1a412320f16c0352022-12-21T23:46:49ZengBMCChinese Medicine1749-85462020-06-0115111210.1186/s13020-020-00345-7The protective effects of liguzinediol on congestive heart failure induced by myocardial infarction and its relative mechanismQi Chen0Dini Zhang1Yunhui Bi2Weiwei Zhang3Yuhan Zhang4Qinghai Meng5Yu Li6Huimin Bian7School of Pharmacy, Nanjing University of Chinese MedicineKey Laboratory on Biosafety, Nanjing Institute of Environmental Sciences, Ministry of Ecology and EnvironmentSchool of Pharmacy, Nanjing University of Chinese MedicineSchool of Pharmacy, Nanjing University of Chinese MedicineSchool of Pharmacy, Nanjing University of Chinese MedicineSchool of Pharmacy, Nanjing University of Chinese MedicineSchool of Medicine and Life Sciences, Nanjing University of Chinese MedicineSchool of Pharmacy, Nanjing University of Chinese MedicineAbstract Background Heart failure (HF) is one of the most common causes of cardiovascular diseases in the world. Currently, the drugs used to treat HF in the clinic may cause serious side effects. Liguzinediol, 2, 5-dimethyl-3, 6-dimethyl-pyrazine, is a compound synthesized after the structural modification of ligustrazine (one active ingredient of Szechwan Lovage Rhizome). We aimed to observe the effects of liguzinediol on preventing HF and explore the related mechanisms. Methods The ligation of left anterior descending coronary artery was operated to established the myocardial infarction (MI) model in Sprague–Dawley rats. Cardiac functions were recorded by echocardiography and hemodynamics. The changes in the Renin–Angiotensin–Aldosterone System (RAAS), inflammation, and oxidative stress were detected by radioimmunoassay and Elisa kits. Western blot and real-time PCR were applied to determine the expressions of the TGF-β1/Smads pathway. Results Firstly, liguzinediol enhanced the systolic and diastolic functions of the heart in MI rats. Liguzinediol improved ventricular remodeling by reducing myocardial cell necrosis, as well as reducing collagen deposition and myocardial fibrosis. Then, liguzinediol suppressed the activation of RAAS, inhibited the synthesis of pro-inflammation factors, and reduced oxidative stress. In the end, liguzinediol also down-regulated the expressions of the TGF-β1/Smads pathway. Conclusions Liguzinediol could alleviate HF caused by MI in rats, and the protective effect was associated with the regulation of the TGF-β1/Smads pathway.http://link.springer.com/article/10.1186/s13020-020-00345-7LiguzinediolHeart failureMyocardial infractionTGF-β1/Smads |
spellingShingle | Qi Chen Dini Zhang Yunhui Bi Weiwei Zhang Yuhan Zhang Qinghai Meng Yu Li Huimin Bian The protective effects of liguzinediol on congestive heart failure induced by myocardial infarction and its relative mechanism Chinese Medicine Liguzinediol Heart failure Myocardial infraction TGF-β1/Smads |
title | The protective effects of liguzinediol on congestive heart failure induced by myocardial infarction and its relative mechanism |
title_full | The protective effects of liguzinediol on congestive heart failure induced by myocardial infarction and its relative mechanism |
title_fullStr | The protective effects of liguzinediol on congestive heart failure induced by myocardial infarction and its relative mechanism |
title_full_unstemmed | The protective effects of liguzinediol on congestive heart failure induced by myocardial infarction and its relative mechanism |
title_short | The protective effects of liguzinediol on congestive heart failure induced by myocardial infarction and its relative mechanism |
title_sort | protective effects of liguzinediol on congestive heart failure induced by myocardial infarction and its relative mechanism |
topic | Liguzinediol Heart failure Myocardial infraction TGF-β1/Smads |
url | http://link.springer.com/article/10.1186/s13020-020-00345-7 |
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