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Protection of H9c2 Myocardial Cells from Oxidative Stress by Crocetin via PINK1/Parkin Pathway-Mediated Mitophagy
Published on: May 26, 2023
Safflower extract inhibiting apoptosis by inducing autophagy in myocardium derived H9C2 cell
Zhisheng Jia1, Yancai Liu1, Huailing Su1
1Department of Cardiology, The Fifth People's Hospital of Jinan City Jinan 250022, Shandong, China.
Insights
Safflower extract inhibits heart cell apoptosis by inducing autophagy, a key cellular process. This finding suggests safflower may offer a novel therapeutic approach for heart failure (HF).
Area of Science:
- Cardiovascular Biology
- Cellular Pathology
- Pharmacology
Background:
- Heart failure (HF) is a global health concern, representing the end stage of various cardiac diseases.
- Progressive loss of cardiac myocytes through apoptosis is a critical factor in HF pathology.
- Identifying novel therapeutic targets to prevent myocyte apoptosis is crucial for HF treatment.
Purpose of the Study:
- To investigate the effect of Safflower extract on Angiotensin II (AngII)-induced apoptosis in H9C2 cardiac myocyte cells.
- To elucidate the mechanism by which Safflower extract exerts its anti-apoptotic effects, focusing on autophagy.
- To evaluate the potential of Safflower extract as a therapeutic agent for heart failure.
Main Methods:
- H9C2 rat myocardium-derived cells were treated with Safflower extract and Angiotensin II (AngII).
- Apoptosis was assessed, and markers of autophagy, such as LC-3II conversion and autophagosome formation, were examined.
- The role of autophagy was confirmed using 3-methyladenine (3MA) to inhibit autophagy and Rapamycin to stimulate it.
- Expression levels of pro-apoptotic genes (BAD and Bax) were analyzed.
Main Results:
- Safflower extract significantly inhibited AngII-induced apoptosis in H9C2 cells.
- Safflower extract treatment promoted autophagy, evidenced by increased LC-3II conversion and autophagosome formation.
- Inhibition of autophagy with 3MA abolished the anti-apoptotic effect of Safflower extract.
- Rapamycin, an autophagy stimulator, also inhibited apoptosis.
- Safflower extract reduced the expression of pro-apoptotic genes BAD and Bax.
Conclusions:
- Safflower extract inhibits apoptosis in cardiac myocyte cells by inducing autophagy.
- The findings highlight the crucial role of autophagy in mediating the cardioprotective effects of Safflower extract.
- Safflower extract demonstrates potential as a novel therapeutic strategy for managing heart failure.
Abstract:
The Heart failure (HF) is considered as the end-stage of various heart disease and associated with high mortality globally. Progressive loss of cardiac myocytes via apoptosis is considered as the most important factor for HF pathology. In this study, we demonstrated that Safflower extract was able to inhibitthe apoptosis inducted by Angiotensin II (AngII) in a ratmyocardium derived cell line H9C2. Further examination of LC-3II conversion and autophagosome formation suggested Safflower extract induced autophagy in treated cell. Inhibition of Safflower extract induced autophagy by 3-methyladenine (3MA) abolished anti-apoptotic function of Safflower extract, while application of autophagy stimulator Rapamycin in H9C2 inhibited apoptosis as well. Moreover, treatment of H9C2 cell with Safflower extract also inhibited expression of pro-apoptotic genes BAD and Bax. In conclusion, our data indicated that Safflower extract inhibit apoptosis via inducing autophagy in myocardium cell and demonstrated the potential as novel therapeutic drug for Heart failure.
