[Protein C activator derived from snake venom protects human umbilical vein endothelial cells against hypoxia-reoxygenation injury by suppressing ROS

• DOI: 10.12122/j.issn.1673-4254.2025.03.19
• Publication Date: 2025-03-20
• Authors: Ming Liao; Wenhua Zhong; Ran Zhang; Juan Liang; Wenxia Xu; Wenjun Wan; Chao Wu; 曙 李
• Keywords: Hypoxia

To investigate the antioxidative mechanism of snake venom-derived protein C activator (PCA) in mitigating vascular endothelial cell injury. Human umbilical vein cells (HUVECs) were cultured DMEM containing 1.0 g/L D-glucose and exposed to hypoxia (1% O2) for 6 h followed by reoxygenation 2 establish a model oxygen-glucose deprivation/reoxygenation (OGD/R). The was treated with μg/mL PCA alone or combination 2-ME2 (a HIF-1α inhibitor) DMOG stabilizer), intracellular production reactive oxygen species (ROS) expression levels HIF-1α, BNIP3, Beclin-1 detected using DCFH-DA fluorescence probe, flow cytometry, Western blotting. OGD/R transfected BNIP3-specific siRNA scrambled control sequence prior treatment, changes expressions BNIP3 ROS examined. In model, treatment significantly upregulated reduced production. effects obviously attenuated co-treatment but augmented stabilizer). knockdown, increased decreased without causing significant expression. Compared HUVECs only, knockdown showed lower higher levels. Snake venom alleviates OGD/R-induced injury upregulating HIF-1α/BNIP3 signaling suppress generation, suggesting its potential as therapeutic agent against oxidative stress pathologies.