Exogenous H2S contributes to recovery of ischemic post-conditioning-induced cardioprotection by decrease of ROS level...

Area of Science:

• Cardiovascular Science
• Cellular Biology
• Biochemistry

Background:

• Hydrogen sulfide (H2S) is a gasotransmitter vital for cardiovascular function.
• Ischemic post-conditioning (PC) protects against hypoxia/reoxygenation (H/R) injury but is ineffective in aging cardiomyocytes.
• The role of H2S in restoring PC cardioprotection in aged cells remains unclear.

Purpose of the Study:

• To investigate if exogenous H2S can restore PC-induced cardioprotection in aging cardiomyocytes.
• To determine if H2S mitigates H/R-induced injury and apoptosis by reducing reactive oxygen species (ROS).

Main Methods:

• Aging cardiomyocytes were induced using d-galactose and subjected to H/R and PC protocols.
• Cell viability, apoptosis, ROS levels, and protein expressions were assessed.
• H2S was supplied using NaHS (a donor), and its effects were compared to ROS and NF-κB inhibitors.

Main Results:

• NaHS treatment protected aging cardiomyocytes against H/R injury, reducing apoptosis and cell damage.
• H2S supplementation decreased ROS levels and key apoptotic markers (caspase-3/9, Cyt c).
• NaHS restored PC efficacy in aging cells, comparable to ROS and NF-κB inhibitors.

Conclusions:

• Exogenous H2S restores PC-induced cardioprotection in aging cardiomyocytes.
• H2S acts by decreasing ROS levels through the down-regulation of NF-κB and JAK2/STAT3 pathways.