Zhang Hui-yun, Yang Jing, Long Xing-nan, He Shao-heng
Department of Pathophysiology, Hainan Medical College, Haikou 571101, China.
Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi. 2011 Aug;27(8):829-31.
To investigate the effect of TNF on release of IL-6, IL-10 and histamine from mast cells and to explore its potential signal transduction pathway.
After stimulation of various concentrations of TNF, the P815 cells were analyzed by cellular activation of signal ELISA(CASE) to detect phosphorylation of ERK, p38 and STAT3, and the supernatants were collected and analyzed by ELISA to quantify release of IL-6, IL-10 and histamine from the cells.
Compared with the untreated control, increased IL-6 release was detected in TNF-stimulated P815 cells (P<0.05). Pretreatment of PD98059 or U0126 inhibited TNF-induced IL-6 release and ERK phosphorylation in P815 cells (P<0.05), whereas pretreatment of SB203580 or AG490 hardly affect IL-6 release, with little effect on phosphorylation of p38 and STAT3 respectively.
TNF induced IL-6 release from P815 cells may involve activation of ERK signalling pathway.
研究肿瘤坏死因子(TNF)对肥大细胞释放白细胞介素-6(IL-6)、白细胞介素-10(IL-10)和组胺的影响,并探讨其潜在的信号转导途径。
用不同浓度的TNF刺激后,通过信号酶联免疫吸附测定法(CASE)分析P815细胞,以检测细胞外调节蛋白激酶(ERK)、p38和信号转导子及转录激活子3(STAT3)的磷酸化情况,并收集上清液,用酶联免疫吸附测定法(ELISA)分析以定量细胞释放的IL-6、IL-10和组胺。
与未处理的对照组相比,在TNF刺激的P815细胞中检测到IL-6释放增加(P<0.05)。用PD98059或U0126预处理可抑制TNF诱导的P815细胞中IL-6释放和ERK磷酸化(P<0.05),而用SB203580或AG490预处理几乎不影响IL-6释放,分别对p38和STAT3的磷酸化影响很小。
TNF诱导P815细胞释放IL-6可能涉及ERK信号通路的激活。