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目的通过肿瘤坏死因子-α(TNF-α)刺激胃癌细胞株SGC7901,探讨p38丝裂原激活的蛋白激酶MAPK(p38MAPK)调控核转录因子(NF)-κB通路在温郁金二萜类化合物C抗炎和诱导胃癌细胞凋亡中的作用。方法将不同浓度的温郁金二萜类化合物C在不同的时间,体外作用于人脐静脉细胞(HUVECs)、胃癌SGC-7901细胞,采用MTT法检测其对两种细胞株的增殖抑制率;采用Annexin V-FITC/PI双染法检测各组胃癌细胞凋亡率;细胞免疫荧光检测p65核转位情况,采用Western blot检测各组p38MAPK/P-p38MAPK、p65/P-p65及Caspase-3/P-Caspase-3蛋白表达量。结果温郁金二萜类化合物C对SGC-7901细胞增殖有明显的抑制作用,并能有效地诱导胃癌细胞SGC-7901凋亡;温郁金二萜类化合物C能一定程度地减少胃癌细胞SGC-7901p65核转位发生;Western blot结果提示,p38MAPK、p65蛋白的表达随着温郁金二萜类化合物C浓度的提高而减少,而Caspase-3蛋白的表达则增加(P<0.05)。结论通过p38MAPK调控p65来激活凋亡执行蛋白Caspase-3是温郁金二萜类化合物C发挥抗炎和抗癌可能的作用机制之一。
Objective To investigate the effect of p38 mitogen-activated protein kinase MAPK (p38MAPK) on the nuclear factor-kappa B (NF-κB) pathway in gastric cancer cell line SGC7901 stimulated by TNF- And induce apoptosis in gastric cancer cells. METHODS Different concentrations of diterpene C from different concentrations were used to treat human umbilical vein cells (HUVECs) and gastric cancer SGC-7901 cells at different times and in vitro. MTT assay was used to detect the inhibitory rate of diterpene C on both cell lines. Annexin The apoptosis rate of gastric cancer cells in each group was detected by V-FITC / PI double staining. The nuclear translocation of p65 was detected by immunofluorescence. The expressions of p38MAPK / P-p38MAPK, p65 / P-p65 and Caspase-3 / P -Caspase-3 protein expression level. Results Wenyujin diterpenoid C could significantly inhibit the proliferation of SGC-7901 cells and induce the apoptosis of SGC-7901 gastric cancer cells. The diterpene C could decrease the nuclear translocation of SGC-7901p65 cells to a certain extent Western blot showed that the expression of p38MAPK and p65 decreased with the increase of the concentration of diterpene C in the warm turmeric and the expression of Caspase-3 increased (P <0.05). Conclusions Caspase-3, an activator of apoptosis through p38MAPK regulation of p65, is one of the possible mechanisms by which warm-green diterpene C exerts its anti-inflammatory and anticancer activities.