Figure 2: Effects of NGR1 on H/R-induced cell death, depolarization of mitochondrial membrane and intracellular ROS accumulation in H9c2 cardiomyocytes. | Scientific Reports

Figure 2: Effects of NGR1 on H/R-induced cell death, depolarization of mitochondrial membrane and intracellular ROS accumulation in H9c2 cardiomyocytes.

From: Cardioprotective effects of Notoginsenoside R1 against ischemia/reperfusion injuries by regulating oxidative stress- and endoplasmic reticulum stress- related signaling pathways

Figure 2

H9c2 cardiomyocytes were incubated with indicated concentration of NGR1 (2.5, 5, 10, 20, 40 and 80 μM) for 24 h and then exposed to 6 h of hypoxia and 12 h of reoxygenation. (a) NGR1 had no toxic effect on cell viability with concentrations under 20 μM; Effects of NGR1 on H/R-induced cell viability were detected by (b) MTT and cell death by (c) extracellular LDH; (d) Intracellular ROS levels evaluated using a FACSCalibur flow cytometer; (e) Bar diagram showing intracellular ROS level in H9c2 cardiomyocytes; (f) Bar graphs and (g) representative images of JC-1 red/green cells and merges showed that NGR1 increased the ratio of red to green fluorescence intensity. #P < 0.05 versus the control group, ##P < 0.01 versus the control group, ###P < 0.001 versus the control group, *P < 0.05 versus the H/R group, **P < 0.01 versus the H/R group, ***P < 0.001 versus the H/R group.

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