Cigarette Smoke Extract and Lipopolysaccharides Induce Pyroptosis in Rats Pulmonary Microvascular Endothelial Cells
Abstract Objective: To investigate the effects of cigarette smoke extract (CSE) and lipopolysaccharide (LPS) on the activity and pyroptosis of pulmonary microvascular endothelial cells (PMVECs). Methods: PMVECs were cultured without treatment or with CSE (1%-25%), LPS, or CSE+LPS. Cell viability was detected using the CCK8 method. Apoptosis was evaluated by flow cytometry. Cell morphology was evaluated using optical microscopy. The content of IL-1β and IL-18 was measured by ELISA. Results: CSE decreased cell viability in a dose-dependent manner. The cells in the CSE+LPS group showed the most obvious cytomorphological changes and the highest pyroptosis rate under the microscope. Flow cytometry showed that the CSE and LPS groups showed higher apoptosis rates than the blank group; the apoptotic rate in the CSE+LPS group was even higher (P<0.01). Compared with the bkank group, the levels of IL-18 and IL-1β in the cell supernatant of the CSE, LPS, and CSE+LPS groups increased significantly, with significant differences (P<0.01). There were no differences between the CSE and LPS groups (P>0.05). Compared with the CSE and LPS groups, the CSE+LPS group had higher IL-18 and IL-1β (P<0.01). Conclusion: The effect of CSE on cell viability is dose-dependent. CSE+LPS can induce cell pyroptosis and increase the levels of inflammatory cytokines in PMVECs. These observations demonstrated that pyroptosis caused by CSE and LPS might play an important role in pulmonary vascular remodeling.