注射用胸腺法新对人肺癌A549细胞凋亡的影响
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篇名: | 注射用胸腺法新对人肺癌A549细胞凋亡的影响 |
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摘要: | 目的:研究注射用胸腺法新对人肺癌A549细胞凋亡的影响。方法:以0(空白对照)、25、50、100、200、400 mg/L注射用胸腺法新作用于肺癌A549细胞24、48、72 h后,用MTT法检测并计算细胞增殖抑制率。以0(空白对照)、50、100 mg/L注射用胸腺法新作用于肺癌A549细胞48 h后,用流式细胞仪检测细胞的凋亡情况,用Western blot法检测凋亡相关蛋白Caspase-3、Bcl-2、Bax的表达和蛋白激酶B(Akt)的磷酸化水平。结果:与空白对照比较,注射用胸腺法新作用后A549细胞的增殖抑制率增加,与浓度和作用时间呈正相关(P<0.05);50、100 mg/L的注射用胸腺法新作用48 h后A549细胞的凋亡率增加(P<0.05);100 mg/L的注射用胸腺法新作用48 h后A549细胞中Caspase-3表达增强、Bcl-2/Bax和Akt磷酸化水平降低(P<0.05)。结论:注射用胸腺法新可通过激活Caspase-3、下调Bcl-2/Bax比例、抑制Akt信号通路来抑制A549细胞增殖,并促进其凋亡。 |
ABSTRACT: | OBJECTIVE: To study the effects of Thymalfasin for injection on the apoptosis of human lung cancer A549 cells. METHODS: After treated with 0 (blank control), 25, 50, 100, 200 and 400 mg/L Thymalfasin for injection for 24, 48 and 72 h, the cell proliferation inhibitory rate was analyzed with MTT and calculated. After treated with 0 (blank control), 50 and 100 mg/L Thymalfasin for injection for 48 h, cell apoptosis was detected by flow cytometry, and the expression of Caspase-3, Bcl-2 and Bax and the phosphorylation level of Akt were deteced by Western blot. RESULTS: Compared with blank control group, proliferation inhibitory rate of A549 cells increased after treated with Thymalfasin for injection, in concentration and time-dependent manner (P<0.05). The apoptotic rate of A549 cells increased after treated with Thymalfasin for injection 50, 100 mg/L for 48 h (P<0.05). The expression of Caspase-3 increased while the Bcl-2/Bax and phosphorylation level of Akt decreased in A549 cells after treated with Thymalfasin for injection 100 mg/L (P<0.05). CONCLUSIONS: Thymalfasin for injection can inhibit the proliferation of A549 cells by activating Caspase-3, decreasing Bcl-2/Bax ratio, inhibiting Akt signal pathway and induce the apoptosis of A549 cells. |
期刊: | 2016年第27卷第7期 |
作者: | 杨兆辉,段瑞祥,杨晶,熊妲妮,郎建敏 |
AUTHORS: | YANG Zhaohui,DUAN Ruixiang,YANG Jing,XIONG Dani,LANG Jianmin |
关键字: | 注射用胸腺法新;人肺癌A549细胞;增殖;凋亡;Akt信号通路 |
KEYWORDS: | Thymalfasin for injection; Human lung cancer A549 cells; Proliferation; Apoptosis; Akt signal pathway |
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