目的探讨烟曲霉孢子对人支气管上皮细胞(16HBE)早期凋亡的影响及其可能机制。方法采用肿瘤坏死因子α(TNF-α)诱导16HBE细胞凋亡,再分别用不同浓度的乳胶珠颗粒、灭活烟曲霉孢子和静息烟曲霉孢子刺激上述细胞,流式细胞仪检测细胞凋亡率的变化,免疫印迹法检测细胞内半胱氨酸天冬氨酸蛋白酶3(caspase-3)的表达。结果TNF-α刺激后16HBE细胞的凋亡率明显增加(P〈0.05)。静息烟曲霉孢子组细胞凋亡率明显下降(P〈0.05),caspase-3表达明显减少(p〈0.05)。静息烟曲霉孢子浓度越高,细胞凋亡率及caspase-3表达越低。乳胶珠颗粒与灭活烟曲霉孢子对16HBE细胞凋亡率及caspase-3表达水平均无明显影响(P〉0.05)。结论烟曲霉孢子可通过调控caspase-3而抑制TNF-α诱导的16HBE细胞早期凋亡,且烟曲霉孢子浓度越高抑制作用越明显。
Objective To investigate the effect of AspergiUus fumigatus conidia on early apoptosis of human bronchial epithelial cells (16HBE), and to explore the possible mechanism thereof. Methods 16HBE cells were challenged with tumor necrosis factor-α (TNF-α) to induce cell apoptosis, then treated by different concentrations of killed or resting Aspergillusfurnigatus conidia or latex beads simultaneously. The apoptosis of 16HBE ceils were detected by flow cytometry, and the expression of caspase-3 was detected by Western blotting. Results The apoptosis of 16HBE ceils increased markedly after TNF-α stimulating (P〈0.05), while the apoptosis was inhibited greatly and caspase-3 secretion decreased following stimulation by resting Aspergillus furnigatus conidia (P〈0.05) in a concentration-dependent manner. Stimulation by latex beads and killed conidia showed no effect on the cell apoptosis and caspase-3 secretion (P〉0.05). Conclusion Aspergillusfurnigatus conidia may inhibit the early apoptosis of 16HBE cells induced by TNF-α in a concentration-dependent manner.