Fig 2: The Mechanism By Which Sevoflurane Induces Pyroptosis In SCLC Cells. Exposure to sevoflurane can lead to an increase in intracellular calcium levels, activating the mitochondrial calcium transporter (MCU) and causing mitochondrial calcium overload. This overload results in increased expression of EFHD1 and triggers excessive production of reactive oxygen species (ROS), as well as enhanced activity of cytochrome c oxidase (CCO). The excessive ROS and the release of cytochrome c promote mitochondrial dysfunction, induce the activation of caspase-1, and ultimately lead to the cleavage of GSDMD, resulting in pyroptosis

Fig 3: EFHD1 Mediates Sevoflurane-Induced Cell Pyroptosis. A q-PCR analysis of EFHD1 overexpression and knockdown (n = 6). B Western blot analysis of EFHD1 protein expression (n = 3). C ROS levels after sevoflurane treatment of EFHD1 overexpression cells (n = 3). D CCO levels after sevoflurane treatment of EFHD1 overexpression cells (n = 6). E ROS levels after sevoflurane treatment of EFHD1 knockdown cells (n = 3). F CCO levels after sevoflurane treatment of EFHD1 knockdown cells (n = 6). G Western blot analysis of cleaved-caspase-1, GSDMD, and EFHD1 protein expression after sevoflurane treatment of EFHD1 overexpression cells (n = 3). H Western blot analysis of cleaved-caspase-1, GSDMD, and EFHD1 protein expression after sevoflurane treatment of EFHD1 knockdown cells (n = 3). *P < 0.05; **P < 0.01