【摘要】：目的探討HBe Ag對(duì)LPS誘導(dǎo)小鼠骨髓源性樹(shù)突狀細(xì)胞(DC)成熟的影響。方法體外誘導(dǎo)C57BL/6小鼠骨髓細(xì)胞分化成未成熟樹(shù)突狀細(xì)胞,經(jīng)CD11c磁珠分選純化后將DCs隨機(jī)分為空白對(duì)照組、LPS刺激組、HBe Ag+LPS刺激組。流式檢測(cè)DC表型變化,混合淋巴反應(yīng)(MLR)檢測(cè)DC促T淋巴細(xì)胞增殖能力,酶聯(lián)免疫法(ELISA)檢測(cè)細(xì)胞上清液中IL-12的分泌水平,Western blot檢測(cè)p38磷酸化水平,并設(shè)置SB203580組為陽(yáng)性對(duì)照探討細(xì)胞IL-12分泌的可能調(diào)節(jié)機(jī)制。結(jié)果 LPS刺激未成熟DC引起細(xì)胞表面MHC-Ⅱ、CD86表達(dá)升高,刺激同種異體淋巴細(xì)胞增殖能力增強(qiáng),IL-12分泌量增高。HBe Ag可抑制LPS促進(jìn)DC表面MHC-Ⅱ、CD86表達(dá)升高和促淋巴細(xì)胞增殖能力增強(qiáng)的作用。LPS刺激DC可引起p38磷酸化水平升高,并呈時(shí)間依賴(lài)性;HBe Ag或SB203580預(yù)處理細(xì)胞再予LPS刺激,磷酸化p38表達(dá)和IL-12分泌較單純LPS刺激組明顯下降。結(jié)論 HBe Ag對(duì)LPS引起的樹(shù)突狀細(xì)胞的成熟有一定的抑制作用,且HBe Ag可能通過(guò)抑制p38MAPK信號(hào)通路下調(diào)LPS誘導(dǎo)的樹(shù)突狀細(xì)胞IL-12的產(chǎn)生。
[Abstract]:Objective to investigate the effect of HBe Ag on (DC) maturation of mouse bone marrow derived dendritic cells induced by LPS. Methods Bone marrow cells of C57BL/6 mice were induced to differentiate into immature dendritic cells in vitro. DCs was randomly divided into blank control group and, HBe Ag LPS stimulation group after DCs was purified by CD11c magnetic beads. The phenotypic changes of DC were detected by flow cytometry, the proliferation ability of T lymphocytes stimulated by DC was detected by mixed lymphoid reaction (MLR), the level of IL-12 secretion in supernatant was detected by enzyme linked immunosorbent assay (ELISA), and the phosphorylation level of p38 was detected by, Western blot. The possible regulation mechanism of IL-12 secretion in SB203580 group was discussed. Results LPS stimulated immature DC increased the expression of MHC- 鈪，

本文編號(hào)：2422035