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. 2023 Jan 6;12(1):140. doi: 10.3390/antiox12010140

Figure 1.

Figure 1

Hyd protects LECs from H2O2-induced oxidative cell death. (A,B) Viability assay showing the dose-dependent effect(s) of Hyd on survival of SRA-hLECs and mLECs. Cultured SRA-hLECs and mLECs were treated with different concentrations of Hyd to determine its nontoxic concentration using MTS assay. The data represent the mean ± S.D. of three independent experiments. Untreated vs. Hyd-treated LECs; * p < 0.05; ** p < 0.001. (C,D) The cell viability of LECs under H2O2-induced oxidative stress was significantly improved with Hyd treatment. Cultured SRA-hLECs and mLECs were exposed to H2O2 in absence or presence of Hyd for 24 h as indicated in Figure 1, and cell viability was performed using MTS assay. Histograms represent the mean ± S.D. value of three independent experiments. * p < 0.05; ** p < 0.001. (E,F) Hyd defends LECs against H2O2-induced cell death by reducing the ROS levels. Hyd-treated and untreated SRA-hLECs and mLECs were exposed to H2O2. Then, 16 h later, ROS levels were quantified with H2-DCF-DA dye method. Histogram represents the mean ± S.D. of three independent experiments. * p < 0.05; ** p < 0.001.