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目的:探讨百里醌对人卵巢癌细胞株OVCAR-3的作用及相关机制。方法:采用不同浓度(0、10μmol/L、20μmol/L和40μmol/L)百里醌处理OVCAR-3细胞。MTT法检测细胞增殖活性,流式细胞仪检测细胞凋亡。RT-PCR和ELISA检测炎症因子白介素-6(IL-6)、白介素1β(IL-1β)和肿瘤坏死因子-α(TNF-α)表达水平。Western blot法检测JAK2、STAT3、p-JAK2、p-STAT3、p-p65和p65表达。结果:百里醌呈浓度依赖性抑制OVCAR-3细胞的增殖和诱导OVCAR-3凋亡,降低IL-6、IL-1β、TNF-α、p-JAK2、p-STAT3和p-p65表达,而对JAK2、STAT3和p65表达无影响。结论:百里醌可抑制OVCAR-3细胞的增殖和诱导凋亡,其作用机制与抑制JAK2/STAT3/p65介导的炎症相关。
Objective: To investigate the effect and its mechanism of beritone on human ovarian cancer cell line OVCAR-3. Methods: OVCAR-3 cells were treated with different concentrations (0, 10μmol / L, 20μmol / L and 40μmol / L) of thioridone. Cell proliferation was measured by MTT assay and apoptosis was detected by flow cytometry. The levels of interleukin-6, interleukin-1β and tumor necrosis factor-α (TNF-α) were detected by RT-PCR and ELISA. Western blot was used to detect the expression of JAK2, STAT3, p-JAK2, p-STAT3, p-p65 and p65. Results: Thymol inhibited the proliferation of OVCAR-3 cells and induced the apoptosis of OVCAR-3 cells in a concentration-dependent manner and decreased the expressions of IL-6, IL-1β, TNF-α, p-JAK2, p-STAT3 and p- While no effect on JAK2, STAT3 and p65 expression. CONCLUSION: Thymol can inhibit the proliferation and induce apoptosis of OVCAR-3 cells. Its mechanism is related to the inhibition of JAK2 / STAT3 / p65-mediated inflammation.