本文關(guān)鍵詞： 不規(guī)則趨化因子 磷脂酰肌醇-激酶 核因子κB IL- 纈沙坦　出處：《中國(guó)醫(yī)科大學(xué)學(xué)報(bào)》2015年03期 　論文類型：期刊論文

【摘要】：目的探討不規(guī)則趨化因子Fractalkine(FKN)、磷脂酰肌醇-3激酶(PI3K)、核因子κB(NF-κB)對(duì)外周血單個(gè)核細(xì)胞(PBMC)IL-6表達(dá)的影響及纈沙坦的干預(yù)作用,研究FKN影響IL-6表達(dá)的信號(hào)轉(zhuǎn)導(dǎo)機(jī)制。方法利用密度梯度離心法分離健康人外周血單個(gè)核細(xì)胞,將提取的PBMC分為7組:空白對(duì)照組、FKN組、LY294002組(PI3K抑制劑)、PDTC組(NF-κB抑制劑)、FKN+纈沙坦組、FKN+LY294002組、FKN+PDTC組,后二組在FKN誘導(dǎo)PBMC細(xì)胞前分別由LY294002、PDTC預(yù)處理。各組PBMC分別在12 h和24 h后,用酶聯(lián)免疫吸附實(shí)驗(yàn)(ELISA)法檢測(cè)各組細(xì)胞培養(yǎng)液中的IL-6表達(dá)。結(jié)果培養(yǎng)12 h后,與對(duì)照組比較,FKN組IL-6明顯降低(P0.05),LY294002組和PDTC組無明顯差異(P0.05);與FKN組比較,FKN+纈沙坦組IL-6明顯降低(P0.05),FKN+LY294002組IL-6明顯升高(P0.05)、FKN+PDTC組IL-6明顯降低(P0.05)。培養(yǎng)24 h后,各組IL-6表達(dá)無明顯差異(P0.05)。結(jié)論 FKN對(duì)人外周血單個(gè)核細(xì)胞IL-6的表達(dá)具有雙向調(diào)節(jié)作用,通過PI3K途徑抑制IL-6的表達(dá),而通過NF-κB途徑促進(jìn)IL-6的表達(dá),總體上FKN可以抑制IL-6的表達(dá)。纈沙坦可增加FKN抑制IL-6表達(dá)的作用。
[Abstract]:Objective to investigate the effects of irregular chemokine Fractalkinesia (FKN), phosphatidylinositol 3 kinase (PI3KN) and nuclear factor- 魏 B (NF- 魏 B) on the expression of IL-6 in peripheral blood mononuclear cells (PBMCs) and the effect of valsartan on the expression of IL-6 in peripheral blood mononuclear cells (PBMCs). To study the signal transduction mechanism of FKN affecting the expression of IL-6. Methods the peripheral blood mononuclear cells (PBMC) of healthy people were isolated by density gradient centrifugation. The extracted PBMC were divided into seven groups: the control group was treated with LY294002 PI3K inhibitor PI3K and the FKN PDTC group with FKN LY294002, the latter two groups were pretreated with LY294002PDTC before FKN induced PBMC cells. PBMC was pretreated at 12 h and 24 h, respectively. Enzyme linked immunosorbent assay (Elisa) was used to detect the expression of IL-6 in the culture medium of each group. Compared with the control group, the IL-6 of the FKN group was significantly lower than that of the control group. There was no significant difference between the PDTC group and the P0.05 group, and the IL-6 of the FKN valsartan group was significantly lower than that of the control group, and the IL-6 of the FKN LY294002 group was significantly higher than that of the control group, and the IL-6 of the P0.05 FKN PDTC group was significantly lower than that of the FKN group, and the IL-6 of the FKN PDTC group was significantly lower than that of the FKN group. Conclusion FKN can regulate the expression of IL-6 in human peripheral blood mononuclear cells and inhibit the expression of IL-6 through PI3K pathway, but promote the expression of IL-6 through NF- 魏 B pathway. In general, FKN inhibited the expression of IL-6, and valsartan increased the inhibitory effect of FKN on IL-6 expression.
【作者單位】： 中國(guó)醫(yī)科大學(xué)附屬第四醫(yī)院心血管內(nèi)科;
【基金】：遼寧省科技廳資助項(xiàng)目(2011404013-6)
【分類號(hào)】：R96

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