홍삼과 사포닌의 호흡기 상피세포에서 전자담배에 의해 유발된 사이토카인과 점소 5AC/5B의 조절

Abstract

Background and Objectives Electronic cigarette (e-cigarette) is a device that generate vaporby heating e-cigarettes liquid. E-cigarette damages the respiratory immune system andrenders the respiratory tract vulnerable to inflammations. However, there are no studies onhow the inflammatory reactions in respiratory epithelial cells caused by e-cigarette occur, andthe effects of Korean red ginseng (KRG) and saponin on inflammation induced by e-cigaretteare unknown. This study aimed to compare the inflammatory reactions caused by e-cigaretteand lipopolysaccharide (LPS), and to investigate the effects of KRG and saponin on cytokineand mucin expression induced by e-cigarette in respiratory epithelial cells. Subjects and Method In bronchoalveolar lavage fluid and lung tissue of mice, the effects ofKRG and saponin on cytokines (interleukin [IL]-1β, IL-6, IL-8) and mucin 5AC/5B(MUC5AC/5B) expression induced by e-cigarette were investigated using real-time polymerasechain reaction, enzyme linked immunosorbent assay, and immunohistochemistry staining. Results Inflammatory cells, cytokines (IL-1β, IL-6, IL-8) and MUC5AC/5B messenger RNAexpression and protein production were increased by e-cigarette, similar to LPS. KRG and saponindecreased the expression of cytokines (IL-1β, IL-6, IL-8) and MUC5AC/5B induced bye-cigarette. KRG and saponin showed effects similar to that of dexamethasone. Conclusion E-cigarette causes inflammation similar to that caused by LPS. KRG and saponinregulate the expression of cytokine and MUC5AC/5B increased by e-cigarette in respiratoryepithelial cells. KRG and saponin may be an effective therapeutic option for inflammatoryresponses induced by e-cigarette in respiratory epithelial cells.