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目的:研究金喜素抑制人肺癌SH-77细胞增殖及诱导其凋亡的作用,并探讨其机制。方法:体外培养肺癌细胞,以20mg·L-1金喜素处理细胞24小时后,MTT法检测金喜素对肺癌细胞增殖的影响;TUNEL法和流式细胞仪检测肺癌细胞凋亡情况以及Caspase-3特异性拮抗剂Ac-DEVD-CHO(50μmol·L)对金喜素诱导凋亡作用的影响;放射性同位素法检测肺癌细胞胞膜蛋白激酶C(PKC)活性。结果:金喜素处理细胞24小时后,肺癌细胞的存活率为59.8%±5.5%,未经金喜素处理的对照组细胞存活率为98.3%±9.4%,两组间有显著差异性(P<0.01);TUNEL法观察到典型的凋亡细胞形态学特征,流式细胞仪检测肺癌细胞凋亡率为14.5%±3.1%,显著高于对照组细胞(P<0.01);Ac-EDVD-CHO和金喜素共同处理细胞24小时其凋亡率为7.1%±1.3%,较单纯金喜素作用组明显降低(P<0.01);肺癌细胞膜PKC活性(pmol/mgprotein·min)为45.3±10.7,较对照组(141.8±30.4)显著降低(P<0.01)。结论:金喜素可抑制SH-77肺癌细胞增殖,并通过Caspase-3途径诱导其凋亡而发挥抗肿瘤作用,其作用机制与降低肺癌细胞PKC活性有关。
Objective: To study the effect of amethasone on inhibiting the proliferation and inducing apoptosis of human lung cancer SH-77 cells and to explore its mechanism. Methods: Lung cancer cells were cultured in vitro, and the cells were treated with 20 mg · L -1 goldSG for 24 hours. MTT assay was used to detect the effect of amestin on the proliferation of lung cancer cells. TUNEL and flow cytometry were used to detect the apoptosis of lung cancer cells and Caspase-3 specificity The effect of antagonist Ac-DEVD-CHO (50μmol·L) on the induction of apoptosis induced by ametrine was investigated by enzyme-linked immunosorbent assay (ELISA). The protein kinase C (PKC) activity of lung cancer cells was detected by radioisotope method. Results: The surviving rate of lung cancer cells was 59.8% ± 5.5% after 24 hours of treatment with AZT, and the survival rate was 98.3% ± 9.4% in the control group without MAP. There was significant difference between the two groups (P <0.01) The morphological characteristics of typical apoptotic cells were observed by TUNEL. The apoptosis rate of lung cancer cells by flow cytometry was 14.5% ± 3.1%, which was significantly higher than that of the control group (P <0.01). Ac-EDVD- Compared with the control group (P <0.01), the apoptosis rate of the cells treated with co-treated cells for 24 hours was 7.1% ± 1.3% ± 30.4) (P <0.01). CONCLUSION: AP can inhibit the proliferation of SH-77 lung cancer cells and induce its apoptosis by Caspase-3 pathway, which may play an antitumor role. Its mechanism may be related to the decrease of PKC activity in lung cancer cells.