Abstract
<title>Abstract</title> <p> Hypoxia-related neuronal injury is a major component of ischemic stroke. 14-3-3γ, encoded by <italic>YWHAG</italic> , participates in neuronal signaling and cellular stress responses, but its role in chemical hypoxia-like injury remains unclear. Here, SH-SY5Y cells were exposed to cobalt chloride (CoCl₂) to establish a hypoxia-like injury model, and <italic>YWHAG</italic> mRNA expression and function were examined by CCK-8 assay, quantitative real-time PCR, Western blotting, DCFH-DA staining, Annexin V-FITC/PI flow cytometry, and siRNA-mediated knockdown. CoCl₂ decreased cell viability in a concentration- and time-dependent manner. Exposure to 400 µM CoCl₂ for 24 h increased <italic>YWHAG</italic> mRNA and 14-3-3γ protein levels and activated apoptosis-related signaling. Under this condition, 14-3-3γ knockdown further increased reactive oxygen species accumulation, apoptosis, the Bax/Bcl-2 ratio, and cleaved caspase-3 expression. These findings indicate that 14-3-3γ is induced as an endogenous response to CoCl₂-triggered hypoxia-like stress and may mitigate oxidative stress and apoptosis in SH-SY5Y cells. </p>