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目的探究苦参碱通过PI3K/Akt信号通路诱导肺癌A549细胞凋亡机制。方法对人肺癌A549细胞进行培养,培养后分为对照组、低浓度组、中浓度组以及高浓度组,对照组中加入生理盐水,分别向低浓度组、中浓度组以及高浓度组,加入浓度为30 mg/L、60 mg/L、120 mg/L的苦参碱,作用48小时后采用流式细胞仪及MTT检测法检测A549细胞凋亡情况,计算生长抑制率,并采用Western Blotting和real time PCR检测PI3K、p-AKT蛋白以及PI3K、AKT mRNA表达水平,比较四组之间的差异。结果高浓度组、中浓度组、低浓度组生长抑制率和凋亡率显著高于对照组(P<0.05),且随着浓度的升高生长抑制率和凋亡率显著升高(P<0.05);高浓度组、中浓度组、低浓度组PI3K、AKT mRNA及PI3K、p-AKT蛋白表达显著低于对照组(P<0.05),且随着浓度的升高PI3K、AKT mRNA及PI3K、p-AKT蛋白表达水平显著降低(P<0.05)。结论苦参碱可诱导肺癌A549细胞凋亡,推测其作用机制与PI3K/Akt信号通路有关。
Objective To investigate the mechanism of matrine inducing lung cancer A549 cell apoptosis through PI3K / Akt signaling pathway. Methods Human lung adenocarcinoma A549 cells were cultured and divided into control group, low concentration group, middle concentration group and high concentration group. The control group was treated with saline, and then added to low concentration group, middle concentration group and high concentration group respectively The concentration of matrine was 30 mg / L, 60 mg / L and 120 mg / L respectively. The apoptosis of A549 cells was detected by flow cytometry and MTT assay after 48 hours. The growth inhibition rate was calculated by Western Blotting Real-time PCR was used to detect the expression of PI3K, p-AKT protein and PI3K, AKT mRNA. The difference between the four groups was compared. Results The growth inhibition rate and apoptosis rate in high concentration group, middle concentration group and low concentration group were significantly higher than those in control group (P <0.05), and the growth inhibition rate and apoptosis rate were significantly increased with the increase of concentration (P < 0.05). The protein expressions of PI3K, AKT and PI3K, p-AKT in high concentration group, middle concentration group and low concentration group were significantly lower than those in control group (P <0.05). With the increase of concentration, PI3K, AKT mRNA and PI3K , P-AKT protein expression was significantly lower (P <0.05). Conclusion Matrine can induce lung cancer A549 cell apoptosis, suggesting that its mechanism of action is related to the PI3K / Akt signaling pathway.