Sevoflurane activates rapamycin signaling to alleviate cardiomyocyte ischemia-reperfusion injury

Abstract

Abstract Background Sevoflurane, as a widely used inhaled general anesthetic, has cardioprotective effects in ischemia-reperfusion injury (I / R). The purpose of this study was to investigate the effect of rapamycin signal target protein on sevoflurane post-processing in H9c2 rat cardiomyocytes. Material and Methods In the experiment use H9c2 rat cardiomyocytes were cultured with sevoflurane. Immunofluorescence staining was performed on H9c2 cardiomyocytes. The morphological structure of mitochondria was analyzed by laser confocal microscope and ImageJ + Mina software. Cardiomyocyte apoptosis was measured by immunofluorescence staining. Western blot was used to detect the expression of rapamycin signal target protein and apoptosis protein in H9c2 cells. Results The experimental results show that sevoflurane post-treatment (SPC) increased the expression of rapamycin signal target protein and alleviated the I / R injury of H9c2 cells (p < 0.05). SPC can promote the mitochondrial fusion of cardiomyocytes by activating rapamycin signal target, reduce mitochondrial division and maintain the normal structure of mitochondria, so as to protect central myocytes from ischemia-reperfusion injury (p < 0.05). Moreover, SPC reduced the apoptosis rate of cardiomyocytes and the expression level of apoptotic proteins caspase-3 and caspase-9 after myocardial I / R injury. The anti apoptotic effect may be the reason for the protective effect of SPC on H9c2 cells (p < 0.05). The use of the inhibitor rapamycin can eliminate this protective effect. Conclusion SPC activates rapamycin signal target to reduce myocardial I / R injury by maintaining myocardial function, promoting mitochondrial fusion and reduce cardiomyocyte apoptosis.