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首页> 外文期刊>Oncology reports >The regulatory effect of the p38 signaling pathway on valdecoxib-induced apoptosis of the Eca109 cell line.
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The regulatory effect of the p38 signaling pathway on valdecoxib-induced apoptosis of the Eca109 cell line.

机译:p38信号通路对伐地考昔诱导的Eca109细胞株凋亡的调节作用。

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Valdecoxib is a second generation selective COX-2 inhibitor that can induce cell apoptosis in a variety of cell types, but its precise regulatory mechanism is unknown. Apoptosis of Eca109 cells and p38 mRNA expression were investigted. The expression of p-p38MAPK, Fas and FasL proteins were detected by immunohistochemical staining and FCM. Valdecoxib increased the apoptosis rate of Eca109 cells. Fas and FasL protein expression was up-regulated in the valdecoxib groups, while SB203580 partly inhibited the valdecoxib-induced overexpression. Valdecoxib increased p38MAPK expression, while SB203580 inhibited the overexpression of this protein and the apoptosis rate decreased. The expression of Fas, FasL and p38MAPK protein were positively correlated with the apoptotic rate. In conclusion, valdecoxib activates the p38MAPK pathway, thus up-regulating expression of the Fas and FasL proteins, which may be one of the mechanisms through which valdecoxib induces apoptosis.
机译:伐地考昔是第二代选择性COX-2抑制剂,可诱导多种细胞类型的细胞凋亡,但其精确调控机制尚不清楚。研究了Eca109细胞的凋亡和p38 mRNA的表达。免疫组织化学染色和流式细胞仪检测p-p38MAPK,Fas和FasL蛋白的表达。伐地考昔可提高Eca109细胞的凋亡率。在valdecoxib组中Fas和FasL蛋白表达上调,而SB203580部分抑制了valdecoxib诱导的过表达。 Valdecoxib增加p38MAPK表达,而SB203580抑制该蛋白的过表达,凋亡率降低。 Fas,FasL和p38MAPK蛋白的表达与细胞凋亡率呈正相关。总之,伐地昔布激活p38MAPK途径,从而上调Fas和FasL蛋白的表达,这可能是伐地昔布诱导细胞凋亡的机制之一。

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