Related Experiment Video
Updated: Dec 30, 2025
Improved Rodent Model of Myocardial Ischemia and Reperfusion Injury
Published on: March 7, 2022
Huoxue Wentong Formula ameliorates myocardial infarction in rats through inhibiting CaMKII oxidation and
Tiantian Liu1, Qingqing Wang1, Kuiwu Yao1
1Department of Cardiology, Guang'anmen Hospital, China Academy of Chinese Medical Sciences, No. 5 Beixian'ge, District of Xi Cheng, Beijing, 100053 China.
Insights
Huoxue Wentong Formula (HXWTF) treatment improved cardiac function in rats with myocardial infarction. It inhibited cardiomyocyte apoptosis and promoted angiogenesis by regulating CaMKII activity.
Area of Science:
- Cardiovascular Research
- Traditional Chinese Medicine
- Molecular Cardiology
Background:
- Myocardial infarction leads to apoptosis and angiogenesis disorders.
- Huoxue Wentong Formula (HXWTF) is a traditional Chinese medicine used for thoracic obstruction and angina pectoris.
- The effects of HXWTF on myocardial ischemia-induced apoptosis and angiogenesis were previously uninvestigated.
Purpose of the Study:
- To investigate the role of HXWTF in myocardial ischemia-induced apoptosis and angiogenesis in a rat model.
- To elucidate the underlying mechanisms of HXWTF action, focusing on CaMKII signaling.
Main Methods:
- Male SD rats underwent coronary artery ligation and were treated with HXWTF or isosorbide mononitrate.
- Cardiac function was assessed using ECG and Echocardiography.
- Histological and immunohistochemical analyses (H&E, CD34/α-SMA) were performed to evaluate pathological changes and angiogenesis.
- In vitro studies assessed cardiomyocyte apoptosis (H9c2) and tube formation (HCMECs).
- Levels of CaMKII (total, phosphorylated, oxidized), CD34, and Bcl-2/Bax ratio were quantified.
Main Results:
- Coronary artery ligation induced cardiac dysfunction, myocardial damage, apoptosis, and angiogenesis impairment.
- HXWTF treatment significantly improved cardiac function, reduced myocardial apoptosis, and restored angiogenic function.
- HXWTF administration down-regulated the oxidation and phosphorylation of CaMKII in ischemic hearts.
- In vitro, HXWTF inhibited apoptosis in H9c2 cells and improved tube formation in HCMECs.
Conclusions:
- HXWTF ameliorates myocardial infarction by inhibiting CaMKII oxidation and phosphorylation.
- HXWTF facilitates angiogenic function and alleviates cardiomyocyte apoptosis.
- Targeting CaMKII activity presents a promising therapeutic strategy for ischemic cardiomyopathy.
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.
More Related Videos
09:53Herbal Munziq Ameliorates Myocardial Ischemia-Reperfusion Injury by Inhibiting Inflammation
Published on: January 10, 2025
05:41Left Anterior Descending Coronary Artery Ligation for Ischemia-Reperfusion Research: Model Improvement via Technical Modifications and Quality Control
Published on: December 16, 2022