Spermidine as a Potential Protective Agents Against Poly(I:C)-Induced Immune Response, Oxidative Stress, Apoptosis,...

Area of Science:

• Veterinary Immunology
• Reproductive Biology
• Molecular Toxicology

Background:

• Viral infections in male yaks cause infertility via Leydig cell apoptosis, immune activation, and oxidative stress.
• Reduced testosterone production is a key consequence of these viral infections.

Purpose of the Study:

• To investigate the protective effects of spermidine (SPD) against dsRNA virus-induced damage in yak Leydig cells (LCs).
• To elucidate the molecular mechanisms underlying SPD's therapeutic potential in restoring male yak fertility.

Main Methods:

• Yak testicular LCs were treated with Poly(I:C) to model viral infection.
• Immune response, apoptosis, oxidative stress, and testosterone levels were assessed in LCs with or without SPD.
• Transcriptomic sequencing was employed to analyze molecular changes.

Main Results:

• Poly(I:C) induced LC dysfunction, decreasing testosterone and increasing immune response, oxidative stress, and apoptosis.
• SPD treatment significantly alleviated immune response and oxidative stress.
• SPD inhibited apoptosis and restored testosterone production in LCs.

Conclusions:

• SPD effectively mitigates dsRNA virus-induced immune response, oxidative stress, and apoptosis in yak LCs.
• SPD demonstrates potential for restoring testosterone production and enhancing male yak fertility post-viral infection.
• Transcriptomic analysis revealed SPD's role in regulating key genes involved in inflammation and apoptosis.