Abstract:Objective: To explore the effect of taxifolin (TAX) on hypoxia/reoxygenation (H/R)-induced myocardial cell injury based on the RhoA/ROCK1 pathway. Methods: CCK-8 was used to screen for the optimal concentration of TAX treatment for H/R induced H9C2. H9C2 cells were separated into normal group, H/R group, H/R+TAX group, H/R+ROCK inhibitor (Y-27632) group, and H/R+TAX+RhoA activator lysophosphatidic acid (LPA) group. Trypan blue staining was performed to detect the survival rate of H9C2 cells. The reagent kit was used to detect the LDH release rate of H9C2 cells. Flow cytometry and TUNEL staining were performed to detect the apoptosis rate of H9C2 cells in each group. DCFH-DA method and ELISA were performed to detect oxidative stress and inflammatory response in H9C2 cells. Western blot was used to detect the expression of RhoA/ROCK1 pathway related proteins in H9C2 cells of each group. Results: Compared with the control group, the survival rate of H9C2 cells in the H/R group was prominently lower (P<0.05). Compared with the H/R group, the survival rate of H9C2 cells was prominently higher in the H/R+TAX 20μmol/L group and the H/R+TAX 40μmol/L group (P<0.05). Compared with the H/R+TAX 40μmol/L group, the H/R+TAX 80μmol/L group showed a prominent decrease in H9C2 cell survival rate (P<0.05). Compared with the control group, the H/R group showed downregulation of H9C2 cell survival rate and GSH-Px, and upregulation of LDH release rate, apoptosis rate, TUNEL positive cell number, ROS fluorescence intensity, MDA, NOX4, IL-6, TNF-α, NLRP3, ICAM-1, RhoA, ROCK1, and p-MLC2/MLC2 (P<0.05). Compared with the H/R group, the H/R+TAX group and H/R+Y-27632 group showed upregulation of H9C2 cell survival rate and GSH-Px, and downregulation of LDH release rate, apoptosis rate, TUNEL positive cell number, ROS fluorescence intensity, MDA, NOX4, IL-6, TNF-α, NLRP3, ICAM-1, ROCK1, and p-MLC2/MLC2 (P<0.05). Compared with the H/R+TAX group, the H/R+TAX+LPA group showed downregulation of H9C2 cell survival rate and GSH-Px, and upregulation of LDH release rate, apoptosis rate, TUNEL positive cell number, ROS fluorescence intensity, MDA, NOX4, IL-6, TNF-α, NLRP3, ICAM-1, RhoA, ROCK1, and p-MLC2/MLC2 (P<0.05). Conclusion: TAX alleviates H/R-induced myocardial cell injury by inhibiting the RhoA/ROCK1 pathway to regulate oxidative stress, inflammatory response, and cell apoptosis.
徐颖, 李丽华, 刘晨, 张宁. 基于RhoA/ROCK1通路探讨花旗松素对缺氧/复氧诱导的心肌细胞损伤的影响[J]. 河北医学, 2026, 32(2): 240-247.
XU Ying, LI Lihua, LIU Chen, et al. Effect of Taxifolin on Hypoxia/Reoxygenation-Induced Myocardial Cell Injury Based on the RhoA/ROCK1 Pathway. HeBei Med, 2026, 32(2): 240-247.