红景天苷对力达霉素诱导人二倍体成纤维细胞衰老的干预作用

Protection of salidroside against lidamycin-induced cellular senescence in human fetal lung fibroblasts 2BS cells

目的:研究红景天苷对力达霉素导致DNA损伤后所诱导的细胞衰老的调节作用。方法:采用MTT法测定药物对人胚肺二倍体成纤维细胞2BS活力的影响;衰老相关的β-半乳糖苷酶染色法观察细胞衰老形态变化;流式细胞术检测细胞周期分布以及γ-H2AX蛋白表达变化;蛋白免疫印迹技术观察p53和p21蛋白表达水平变化。结果:较低浓度(低于0.1 nmol.L-1)力达霉素能够抑制2BS细胞增殖,诱导β-半乳糖苷酶染色率显著升高和G2/M期阻滞,并使DNA损伤相关的γ-H2AX蛋白以及p53和p21蛋白表达升高。红景天苷能够显著干预力达霉素诱导的上述细胞衰老样表型及相关分子信号变化。结论:红景天苷能够抑制基因毒药物所致DNA损伤及其诱导的细胞衰老。

Objective ： To observe the regulation action of salidroside on cellular senescence of human fetal lung fibroblasts 2BS cells induced by lidamycin （LDM）-initiated DNA damage. Methods： Cellular viability was measured with MTT method, and morphological changes were observed by senescence associated β-gal （SA-β-gal） staining. The Cell cycle distribution and γ-H2AX expression were then analyzed by FACS. p53 and p21 expressions were observed by western blotting. Results： LDM of （as low as 0. 1 nmol. L^-1） induced growth arrest and G2/M cell cycle arrest in 2BS cells. Other senescence markers such as SA-β-gal staining were significantly increased upon LDM exposure. Furthermore, DNA damage associated γ-H2AX and p53/p21 protein levels were enhanced by the DNA damaging agent. However, salidroside was found to significantly inhibit senescence-like phenotypes and molecular changes induced by LDM as mentioned above. Conclusion： Salidroside may protect against lidamycin-induced DNA damage and cellular senescence in 2BS cells.