Related Experiment Video
Updated: Apr 20, 2026
08:22
In vitro Assessment of Myocardial Protection following Hypothermia-Preconditioning in a Human Cardiac Myocytes Model
Published on: October 27, 2020
3.5K
Picroside Ⅱ inhibits hypoxia/reoxygenation-induced cardiomyocyte apoptosis by ameliorating mitochondrial function
Jian-Zhe Li1, Shu-Yi Yu2, Dan Mo3
1Department of Pharmacy, Ruikang Hospital, Guangxi University of Chinese Medicine, Nanning, Guangxi 530011, P.R. China.
International Journal of Molecular Medicine
|November 26, 2014
Summary
Picroside II protects heart cells from damage by reducing reactive oxygen species (ROS) and improving mitochondrial function during hypoxia/reoxygenation injury. This study clarifies its mechanism in preventing cardiomyocyte apoptosis.
Area of Science:
- Cardiovascular Research
- Mitochondrial Biology
- Cellular Apoptosis
Background:
- Mitochondrial dysfunction induced by reactive oxygen species (ROS) is a key factor in cardiomyocyte apoptosis during myocardial ischemia/reperfusion (I/R) injury.
- Picroside II, derived from Picrorhiza scrophulariiflora, shows potential cardioprotective effects against hypoxia/reoxygenation (H/R) but its mechanism remains unclear.
Purpose of the Study:
- To investigate the protective effects of Picroside II against H/R-induced cardiomyocyte apoptosis.
- To elucidate the underlying mechanism of Picroside II's cardioprotective action.
Main Methods:
- H9c2 rat cardiomyocyte cell line was treated with Picroside II (100 µg/ml) for 48 hours before H/R.
- Assessed apoptosis, mitochondrial permeability transition pore (mPTP) opening, mitochondrial membrane potential, cytochrome c release, and caspase-3 activity.
Main Results:
- Picroside II significantly inhibited H/R-induced cardiomyocyte apoptosis.
- Picroside II decreased mPTP opening, increased mitochondrial membrane potential, and reduced cytochrome c release.
- Picroside II downregulated caspase-3 expression/activity and decreased ROS production.
Conclusions:
- Picroside II ameliorates mitochondrial function by reducing ROS production, thereby inhibiting H/R-induced cardiomyocyte apoptosis.
- Picroside II demonstrates significant cardioprotective effects against H/R injury through mitochondrial protective mechanisms.
