Prdx1 alleviates cardiomyocyte apoptosis through ROS-activated MAPK pathway during myocardial ischemia/reperfusion...

Area of Science:

• Cardiovascular Research
• Cellular Biology
• Oxidative Stress Mechanisms

Background:

• Myocardial ischemia reperfusion injury (MIRI) impairs heart function recovery due to apoptosis.
• Oxidative stress is a key factor in MIRI-induced cardiomyocyte apoptosis.
• The role of Peroxiredoxin 1 (Prdx1) in MIRI remains largely unknown.

Purpose of the Study:

• To investigate the expression and function of Prdx1 in MIRI.
• To elucidate the protective mechanisms of Prdx1 against MIRI-induced apoptosis.
• To explore the relationship between Prdx1, oxidative stress, and the MAPK pathway in MIRI.

Main Methods:

• Establishment of a rat MIRI model and in vitro H9c2 cell hypoxia/reoxygenation (H/R) model.
• Assessment of Prdx1 protein levels, apoptosis, and MAPK pathway activation (p38, JNK).
• Utilized specific inhibitors (SB203580, SP600125) and a reactive oxygen species (ROS) scavenger (NAC).

Main Results:

• Prdx1 protein levels were elevated in MIRI models and associated with cardiomyocyte apoptosis.
• H/R treatment increased p38 and JNK activation and apoptosis, which were ameliorated by Prdx1.
• Prdx1 inhibited H/R-induced apoptosis by down-regulating p38 and JNK activation, with ROS as an upstream regulator.

Conclusions:

• Prdx1 plays a protective role in MIRI by inhibiting oxidative stress and apoptosis.
• Prdx1 exerts its protective effects through the suppression of the MAPK signaling pathway.
• Reactive oxygen species are critical upstream mediators of apoptosis in H/R-induced MIRI.