[Hyperoside protects mouse spermatocytes GC-2 cells from oxidative damage by activating the Keap1/Nrf2/HO-1 pathway]

Area of Science:

• Oxidative Stress Biology
• Cellular Toxicology
• Natural Product Chemistry

Background:

• Hydrogen peroxide (H₂O₂) induces oxidative damage in mouse spermatocyte GC-2 cells.
• Oxidative stress is implicated in male infertility.
• The Keap1/Nrf2/HO-1 pathway is a key regulator of cellular antioxidant defense.

Purpose of the Study:

• To investigate the protective effects of hyperoside (Hyp) against H₂O₂-induced oxidative damage in GC-2 cells.
• To elucidate the role of the Keap1/Nrf2/HO-1 signaling pathway in hyperoside's protective mechanism.

Main Methods:

• GC-2 cells were treated with hyperoside or N-acetylcysteine (NAC) before exposure to H₂O₂.
• Cell viability (CCK-8 assay), apoptosis (flow cytometry), antioxidant enzyme activities (SOD, GSH-PX, CAT), and lipid peroxidation (MDA) were assessed.
• Western blotting, RT-qPCR, and immunofluorescence were used to analyze the Keap1/Nrf2/HO-1 pathway components and Nrf2 nuclear translocation.

Main Results:

• H₂O₂ exposure reduced cell viability, antioxidant enzyme activity, and increased apoptosis and MDA levels.
• Hyperoside treatment significantly improved cell viability, enhanced antioxidant defenses, and reduced apoptosis and MDA.
• Hyperoside upregulated Nrf2 and HO-1 expression, decreased Keap1 expression, and promoted Nrf2 nuclear translocation.

Conclusions:

• Hyperoside demonstrates significant protective effects against H₂O₂-induced oxidative damage in GC-2 cells.
• The protective mechanism of hyperoside involves the activation of the Keap1/Nrf2/HO-1 signaling pathway.
• Hyperoside shows potential as a therapeutic agent for conditions involving oxidative stress in spermatocytes.