Fig. 5

Activation of S1R attenuates cellular oxidative stress levels and reduces apoptosis in vitro. A Schematic protocol for Flv, BD1047, DOX, siRNA and BAPTA-AM treatment in vitro. B Apoptosis measurement by flow cytometry showed that activation of S1R reduced apoptosis. C Western blot showed activation of S1R reduced cardiomyocyte apoptosis. D The statistical analysis diagrams of apoptosis rate (n = 3). E The statistical analysis diagrams of Bcl2, Bax protein level relative to GAPDH (n = 3). F, G DCFH showed that stimulation of S1R reduced ROS production in cardiomyocytes (n = 3). H Immunofluorescence results showed decreased expression of S1R in cells given DOX. I Activation of S1R inhibited PERK and IP3R-VDAC1-MCU signaling pathways and alleviated endoplasmic reticulum stress and mitochondrial damage (n = 3). J The statistical analysis diagrams of immunofluorescence staining reflecting S1R expression (n = 3). K The statistical analysis diagrams of IP3R, S1R, Bip, PERK, p-PERK, eIF2α, p-eIF2α, ATF4, VDAC1, and MCU protein expression relative to GAPDH in cardiomyocyte (n = 3). *p < 0.05; **p < 0.01; ***p < 0.005; ****p < 0.001