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目的胰岛素样生长因子-1(IGF-1)具有促进细胞分化、抑制细胞凋亡等多种生物学活性。该研究旨在探讨IGF-1对高氧诱导的A549细胞凋亡的影响及其抗凋亡机制。方法将传代培养的A549细胞暴露于高氧环境,并以不同浓度IGF-1(1、10、100 ng/mL)干预48 h,采用四甲基偶氮唑蓝(MTT)法检测细胞存活率,Annexin V-FITC/PI双染流式细胞术检测细胞凋亡变化,同时用流式细胞仪检测凋亡调控相关蛋白(Bax、Bcl-2)表达水平的变化。结果高氧组细胞存活率为(51±3)%,IGF-1干预组细胞存活率随着IGF-1药物浓度的递增逐渐升高,中、高剂量IGF-1干预组细胞存活率分别为(64±3)%和(88±4)%,与高氧组相比,差异均有统计学意义(P<0.05)。高氧组A549细胞凋亡率为(38.3±5.4)%,较空气组(2.4±0.9)%明显增多;高氧组Bcl-2的蛋白表达水平为(72±5)%,较空气组(91±4)%明显下降;高氧组Bax的表达水平为(54±6)%,较空气组(3±2)%明显升高,差异均有统计学意义(P<0.05)。与高氧组比较,IGF-1干预组细胞凋亡率随着药物浓度的增加逐渐下降,分别为(16.1±4.7)%、(9.2±2.8)%和(6.9±2.5)%,差异有统计学意义(P<0.05)。与高氧组比较,IGF-1干预组细胞Bcl-2的表达逐渐增高,分别为(79±4)%、(94±4)%和(100±5)%,而Bax的表达逐渐下降,分别为(26±4)%、(5±2)%和(4±2)%,差异均有统计学意义(P<0.05)。结论高氧明显抑制A549细胞的增殖,促进其凋亡;IGF-1具有促进A549细胞增殖,通过调节凋亡调控蛋白Bcl-2和Bax表达,抑制高氧诱导的A549细胞凋亡的作用。
Purpose IGF-1 has many biological activities such as promoting cell differentiation and inhibiting apoptosis. This study aimed to investigate the effect of IGF-1 on apoptosis of A549 cells induced by hyperoxia and its anti-apoptotic mechanism. Methods A549 cells exposed to hyperoxia were exposed to different concentrations of IGF-1 (1, 10, 100 ng / mL) for 48 h. Cell viability was detected by MTT assay. , Annexin V-FITC / PI double staining flow cytometry was used to detect the change of apoptosis. At the same time, the expression of Bax and Bcl-2 was detected by flow cytometry. Results The survival rate of cells in hyperoxia group was (51 ± 3)%. The cell survival rate of IGF-1 intervention group increased gradually with the increasing of IGF-1 concentration. The cell survival rates of medium- and high-dose IGF- (64 ± 3)% and (88 ± 4)%, respectively, which were significantly different from those in hyperoxia group (P <0.05). The apoptosis rate of A549 cells in hyperoxia group was (38.3 ± 5.4)%, which was significantly higher than that in air group (2.4 ± 0.9)%. The protein expression of Bcl-2 in hyperoxia group was (72 ± 5)%, 91 ± 4)%, while the expression of Bax in hyperoxia group was (54 ± 6)% higher than that in air group (3 ± 2)%, the difference was statistically significant (P <0.05). Compared with hyperoxia group, apoptosis rate of IGF-1 intervention group decreased gradually with the increase of drug concentration (16.1 ± 4.7%, 9.2 ± 2.8% and 6.9 ± 2.5%, respectively) Significance (P <0.05). Compared with the hyperoxia group, the expression of Bcl-2 in the IGF-1 intervention group was (79 ± 4)%, (94 ± 4)% and (100 ± 5)%, respectively, while the expression of Bax decreased gradually (26 ± 4)%, (5 ± 2)% and (4 ± 2)%, respectively. The differences were statistically significant (P <0.05). CONCLUSION: Hypoxia can significantly inhibit the proliferation and promote the apoptosis of A549 cells. IGF-1 can promote the proliferation of A549 cells and inhibit the apoptosis of A549 cells by regulating the expression of Bcl-2 and Bax.