Qi-Tai-Suan, an oleanolic acid derivative, ameliorates ischemic heart failure via suppression of cardiac apoptosis, inflammation and fibrosis.
10.1016/S1875-5364(22)60156-0
- Author:
Ming QIAN
1
;
Zhi-Qi FENG
1
;
Ru-Nan ZHENG
1
;
Kai-Wen HU
1
;
Jia-Ze SUN
1
;
Hong-Bin SUN
2
;
Liang DAI
3
Author Information
1. Jiangsu Key Laboratory of Drug Discovery for Metabolic Disease, State Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing 210009, China.
2. Jiangsu Key Laboratory of Drug Discovery for Metabolic Disease, State Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing 210009, China. Electronic address: hongbinsun@cpu.edu.cn.
3. Jiangsu Key Laboratory of Drug Discovery for Metabolic Disease, State Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing 210009, China. Electronic address: dailiang1993@yeah.net.
- Publication Type:Journal Article
- Keywords:
Apoptosis;
Fibrosis;
Inflammation;
Ischemic heart failure;
Qi-Tai-Suan
- MeSH:
Animals;
Apoptosis;
Fibrosis;
Heart Failure/drug therapy*;
Inflammation/drug therapy*;
Male;
Mice;
Mice, Inbred C57BL;
Myocardial Ischemia/pathology*;
Oleanolic Acid/pharmacology*
- From:
Chinese Journal of Natural Medicines (English Ed.)
2022;20(6):432-442
- CountryChina
- Language:English
-
Abstract:
Although anti-thrombotic therapy has been successful for prevention of deaths from acute myocardial infarction (MI), by far, there are few preventive and therapeutic options for ischemic heart failure (IHF) after MI. Qi-Tai-Suan (QTS) is an oleanolic acid (OA) derivative which once underwent a clinical trial for treating hepatitis. In this study, we investigated the potential cardioprotective effect of QTS on IHF. IHF mouse model was constructed by coronary artery ligation in male C57BL/6J mice, and the protective effects of QTS on IHF were examined by echocardiography measurement, histological and TUNEL analysis, etc. We found that QTS exhibited promising cardioprotective effect on IHF. QTS treatment significantly improved cardiac function of IHF mice and the symptoms of heart failure. Notably, QTS had much better oral bioavailability (F = 41.91%) in mice than its parent drug OA, and took effects mainly as its original form. Mechanistically, QTS ameliorated ischemic heart failure likely through suppression of cardiac apoptosis, inflammation and fibrosis. Taken together, QTS holds great promise as a preventive and therapeutic agent for ischemic heart failure and related diseases.
