Research shows FGF1 improves Bcl-2 levels and reduces apoptosis in H9c2 cells, suggesting potential therapeutic benefits against oxidative stress.
The goal of this research was to reveal the protective effect and mechanism of fibroblast growth factor-1 (FGF1) on oxidative stress injury of H9c2 cells induced by hydrogen peroxide (H2O2). The effects of various concentrations of H2O2 and FGF1 on the activity of H9c2 cells were analyzed by Real Time Cell Analysis (RTCA). The content of ROS, calcium ion, mitochondrial membrane potential and apoptosis were detected by fluorescence probe, the mRNA expression of Bcl-2, Bax and Caspase-3 were detected by real-time PCR to evaluate whether FGF1 has ability to resist the apoptosis of cardiomyocytes caused by oxidative damage. The results showed that the proliferation of H9c2 cells could be inhibited after being treated with 200 μM H2O2 for 12 h, and 100 μg/ml FGF1 could increase the proliferation rate of H9c2 cells, mitochondrial membrane potential and the mRNA expression of Bcl-2, and reduce the ROS accumulation, the level of apoptosis, the content of intracellular calcium and the mRNA expression of Bax and Caspase-3 caused by H2O2. The results showed that FGF1 could regulate oxidative stress by improving mitochondrial function and inhibit the H2O2-induced apoptosis in H9c2 cells.
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Chu et al. (2020) studied this question.
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