Back to Search
Start Over
Huoxue Wentong Formula ameliorates myocardial infarction in rats through inhibiting CaMKII oxidation and phosphorylation.
- Source :
- Chinese Medicine; 1/10/2020, Vol. 15 Issue 1, p1-12, 12p
- Publication Year :
- 2020
-
Abstract
- Background: The Chinese medicine Huoxue Wentong Formula (HXWTF) was used to treat thoracic obstruction and angina pectoris in clinic, which has not been investigated in myocardial ischemia-induced apoptosis and angiogenic function. Here we aimed to investigate the roles of HXWTF in rats with myocardial ischemia-induced apoptosis and angiogenesis disorders, as well as to reveal the potential mechanisms. Methods: Male SD rats were subjected to coronary artery ligation followed by HXWTF (420, 840 and 1680 mg/kg/day, p.o.) or isosorbide mononitrate (6.3 mg/kg/day, p.o.) treatment for 4 weeks. Electrocardiogram (ECG) and Echocardiography (ECHO) were used to measure cardiac function. Hematoxylin and eosin (H&E) staining and CD34/α-SMA immunohistochemical staining were performed to observe the ischemic heart sections pathological changes and angiogenesis. Then, the effects on cardiomyocyte apoptosis of H9c2 and tube formation of HCMECs were observed, as well as the changes in the levels of total calmodulin dependent protein kinase II (t-CaMKII), phosphorylated CaMKII (p-CaMKII), oxidized CaMKII (ox-CaMKII), CD34, and Bcl-2/Bax ratio were detected. Results: Rats with coronary artery ligation exhibited abnormal cardiac function, enlarged myocardial space, disorderly arranged myocardial fibers, inflammatory cells infiltrated, and aggravated myocardial cell apoptosis, along with angiogenesis dysfunction. The expressions of CD34, p-CaMKII, and ox-CaMKII were elevated and Bcl-2/Bax ratio was diminished in ischemic hearts and H/SD-treated H9c2 or HCMECs, while HXWTF treatment completely rescued angiogenic dysfunction, inhibited cardiomyocyte apoptosis, and down-regulated cardiac CaMKII oxidation and phosphorylation activities. Conclusion: Our study demonstrates that HXWTF improves myocardial infarction possibly through inhibiting CaMKII oxidation and phosphorylation levels, facilitating angiogenic function and alleviating cardiomyocyte apoptosis. Thus, therapeutics targeting CaMKII activities may be a promising strategy for rescuing ischemic cardiomyopathy. [ABSTRACT FROM AUTHOR]
- Subjects :
- ANIMAL experimentation
ANTIGENS
APOPTOSIS
BENZOPYRANS
CARDIOVASCULAR system
CORONARY arteries
DIURETICS
ECHOCARDIOGRAPHY
ELECTROCARDIOGRAPHY
GENE expression
HEART cells
HEART function tests
HERBAL medicine
IMMUNOHISTOCHEMISTRY
INFLAMMATORY mediators
CHINESE medicine
MYOCARDIAL infarction
MYOCARDIUM
OXIDATION-reduction reaction
PHOSPHORYLATION
PHOSPHOTRANSFERASES
RATS
STAINS & staining (Microscopy)
FLUORESCENT dyes
PATHOLOGIC neovascularization
DRUG administration
DRUG dosage
PHARMACODYNAMICS
Subjects
Details
- Language :
- English
- ISSN :
- 17498546
- Volume :
- 15
- Issue :
- 1
- Database :
- Complementary Index
- Journal :
- Chinese Medicine
- Publication Type :
- Academic Journal
- Accession number :
- 141150518
- Full Text :
- https://doi.org/10.1186/s13020-020-0285-2