[Hydrogen Sulfide Ameliorates Myocardial Injury Caused by Sepsis Through Suppressing ROS-Mediated Endoplasmic...

Area of Science:

• Cardiovascular Research
• Sepsis Pathophysiology
• Oxidative Stress and ER Stress

Background:

• Sepsis can lead to myocardial injury, characterized by oxidative stress and endoplasmic reticulum stress (ERS).
• Hydrogen sulfide (H ₂S) plays a role in cellular protection, but its specific effects on sepsis-induced cardiac dysfunction remain under investigation.

Purpose of the Study:

• To investigate the protective effects of hydrogen sulfide (H ₂S) against myocardial injury in a rat model of sepsis.
• To elucidate the mechanisms involving reactive oxygen species (ROS)-mediated endoplasmic reticulum stress (ERS) and cardiomyocyte apoptosis.

Main Methods:

• A cecal ligation and puncture (CLP) model was used to induce sepsis in Sprague-Dawley rats.
• Rats were treated with sodium hydrosulfide (NaHS). Cardiac function, oxidative stress markers (LDH, MDA, GSH), H ₂S levels, ER stress markers (p-PERK, p-eIF2α, IRE1α, ATF4, CHOP), and cardiomyocyte apoptosis were assessed.

Main Results:

• Sepsis led to decreased cardiac function, elevated ROS, increased oxidative stress, and upregulated ER stress markers, alongside reduced endogenous H ₂S production and increased cardiomyocyte apoptosis.
• NaHS treatment improved cardiac function, reduced oxidative and ER stress, increased endogenous H ₂S levels, and significantly decreased cardiomyocyte apoptosis.

Conclusions:

• Hydrogen sulfide (H ₂S) exerts a protective effect against sepsis-induced myocardial injury.
• H ₂S mitigates cardiac dysfunction by inhibiting ROS-mediated endoplasmic reticulum stress (ERS), thereby reducing cardiomyocyte apoptosis.