Chemerin promotes H<sub>2</sub>O<sub>2</sub>-induced apoptosis via regulation of the ERK1/2 signaling pathway in bovine ovarian granulosa cells

Extensive evidence indicates that oxidative stress plays an important role in animal reproduction. Chemerin, an adipose hormone found in tissues such as the pituitary gland, placenta, and ovary, plays a role in regulating energy metabolism and reproductive functions. The specific mechanism by which it regulates reproduction, however, remains unclear. This study aimed to determine the effects of chemerin on hydrogen peroxide (H₂O₂)-induced apoptosis in bovine ovarian granulosa cells (BGCs). The results showed that H₂O₂ treatment significantly promoted oxidative stress and apoptosis, which were further enhanced by chemerin. Silencing chemerin reverses the expression of apoptosis-related genes and proteins (Bax, Bcl-2, and Caspase-3), and reduces the apoptosis rate, suggesting that chemerin increases H₂O₂-induced apoptosis. In addition, chemerin enhanced the activation of extracellular-signal-regulated kinases (ERK) 1/2, which was reversed by U0126 co-treatment, and accompanied by the increases of apoptosis, indicating that chemerin promoted H₂O₂-induced apoptosis partially through the ERK1/2 pathway. In summary, these results suggest that chemerin may enhance H₂O₂-induced BGCs apoptosis by activating the ERK1/2 pathway, providing a theoretical basis for exploring the regulatory relationship between fat-secreted factors and animal reproductive performance.