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目的观察氢硫酸钠(Na HS)对脂多糖(LPS)诱导的A549肺癌细胞损伤的影响并探讨其可能机制。方法 A549细胞分为对照组、LPS处理组、Na HS处理组和LPS联合Na HS处理组。处理24 h后,采用ELISA测定培养液中C反应蛋白(CRP)的含量;MTT法与乳酸脱氢酶(LDH)法测定细胞损伤情况;测定A549细胞单层模型的跨上皮电阻(TER)值;免疫荧光染色法测定A549细胞中闭锁小带蛋白1(ZO-1)的分布情况。结果对照组与Na HS处理组比较,CRP的水平、TER值、细胞活力和ZO-1表达与分布情况无显著性差异;与对照组相比,LPS处理组中的CRP水平明显升高、TER值显著减少、细胞活力下降、细胞膜ZO-1表达减少且边界不清;与LPS处理组相比,LPS联合Na HS处理组中的CRP水平明显降低、TER值增加、细胞活力增加,ZO-1在细胞膜处的表达增强且分布情况部分恢复。结论 Na HS通过增强A549细胞活力、降低CRP水平、增加TER值并增加ZO-1表达抑制LPS诱导的肺损伤。
Objective To investigate the effect of sodium hydrosulfite (NaHS) on lung injury induced by lipopolysaccharide (LPS) in A549 cells and to explore its possible mechanism. Methods A549 cells were divided into control group, LPS treatment group, Na HS treatment group and LPS combined with Na HS treatment group. After treatment for 24 h, the content of C-reactive protein (CRP) in the culture medium was measured by ELISA. The cell damage was measured by MTT assay and lactate dehydrogenase (LDH) assay. The trans-epithelial resistance (TER) Immunofluorescence staining was used to determine the distribution of ZO-1 in A549 cells. Results There was no significant difference in the levels of CRP, TER, cell viability and the expression and distribution of ZO-1 between the control group and Na HS group. Compared with the control group, the levels of CRP in the LPS group were significantly increased, and the levels of TER Compared with LPS treatment group, the levels of CRP in LPS group and Na HS treatment group were significantly decreased, TER value was increased, cell viability was increased, ZO-1 expression was significantly decreased, cell viability was decreased, cell membrane ZO-1 expression was reduced and the border was unclear; The expression at the cell membrane is enhanced and the distribution is partially restored. Conclusion NaHS can inhibit the LPS-induced lung injury by increasing the viability of A549 cells, decreasing the level of CRP, increasing the TER value and increasing the expression of ZO-1.