多聚左旋精氨酸诱导NCI-H292细胞凋亡及其可能机制的分析

Role of poly-L-arginine in inducing apoptosis of NCI-H292 cell lines and the possible underlying mechanism

目的观察多聚左旋精氨酸(poly-L-arginine,PLA)诱导气道上皮细胞NCI-H292凋亡以及对细胞内BCL-2/Bax、Caspase 3表达的影响,从而揭示PLA参与哮喘气道损伤的机制。方法按PLA浓度不同分为对照组、10 mg/L组、20 mg/L组、40 mg/L组、60 mg/L组,流式细胞仪检测各组PLA作用24 h后NCI-H292细胞凋亡率;电镜下观察60 mg/L组PLA作用24 h后NCIH292细胞凋亡形态学改变;Western blot法检测各组PLA作用24 h后NCI-H292细胞内Bax、BCL-2及活性Caspase 3的表达。结果各组NCI-H292细胞凋亡率分别为(4.97±0.17)%、(7.82±0.21)%、(11.99±0.21)%、(29.52±0.55)%、(55.23±0.67)%(P<0.05);电镜下PLA作用后NCI-H292细胞呈明显凋亡改变;Western blot检测出细胞中BCL-2/Bax表达降低(P<0.05),活性Caspase 3表达增加(P<0.05)。结论 PLA能引起气道上皮细胞凋亡,并下调BCL-2/Bax表达,上调活性Caspase3表达。

Purpose To study the function of poly-L-arginine in inducing the apoptosis of NCI-H292 cells and its influence on the ex- pression of BCL-2/Bax and Caspase 3, then to further reveal the mechanism of airway damage in asthma. Methods NCI-H292 cells were grouped into control group, 10 mg/L PLA group, 20 mg/L PLA group, 40 mg/L PLA group and 60 mg/L PLA group. The apop- tosis rates of NCI-H292 cells of each group after PLA 24-hours-work were detected by flow cytometry, and the morphological changes of apoptosis in NCI-H292 cells among 60 mg/L PLA group were observed by electron microscope. The expression of the Bax, BCL-2 and cleaved Caspase 3 of each group was detected by Western blot. Results The apoptosis rates of NCI-H292 cells in each group respec- tively were （4. 97± O. 17） %, （7. 82 ± O. 21 ） %, （ 11.99 ± 0. 21 ） %, （ 29. 52 ± 0. 55 ） %, （ 55.23 ± 0. 67） %, （ P 〈 O. 05 ）. The apoptosis changes of NCI-H292 cells induced by PLA was significant under electron microscope, and the expression of BCL-2/Bax in NCI-H292 cells induced by PLA was statistically decreased （ P 〈 0. 05 ） , and the expression of cleaved Caspase 3 was statistically in- creased （ P 〈 0.05 ）. Conclusion PLA can cause the apoptosis of airway epithelial cell by downregulating the expression of BCL-2/ Bax expression and upregulating the expression of cleaved Caspase 3.