發(fā)布時間：2018-03-22 01:17

  本文選題：枯否細胞　切入點：人間充質(zhì)干細胞　出處：《安徽醫(yī)科大學(xué)學(xué)報》2016年01期 　論文類型：期刊論文

【摘要】：目的采用脂多糖(LPS)誘導(dǎo)大鼠枯否細胞(KCs)發(fā)生極化改變,之后用人臍帶血間充質(zhì)干細胞(huM SCs)與LPS誘導(dǎo)的KCs在Transwell內(nèi)共培養(yǎng),以觀察huM SCs對KCs極化偏移的調(diào)節(jié)作用。方法實驗分為KCs組、KCs+LPS組、KCs+LPS+MSCs組。對各組的白介素-4(IL-4)、腫瘤壞死因子(TNF-α)、白介素-10(IL-10)、白介素-6(IL-6)等上清因子采用ELISA法進行檢測;誘導(dǎo)型一氧化氮合酶(iNOS)、精氨酸酶-1(Arg-1)、信號傳導(dǎo)與轉(zhuǎn)錄激活因子3、6(STAT-3、STAT-6)、核因子kappaB(NF-κB)用Western bolt進行檢測,同時用熒光實時定量PCR(qRT-PCR)對以上結(jié)果進行驗證。結(jié)果 KCs+LPS組促炎因子TNF-α、IL-6分泌增加,KCs+LPS+MSCs組抑炎因子IL-10、IL-4分泌增加;而Western blot檢測表明,KCs+LPS組中iN OS升高,NF-κB p65入核增高;而KCs+LPS+MSCs組高表達Arg-1,同時pS TAT-3、pS TAT-6表達增加。結(jié)論 huM SCs能誘導(dǎo)已經(jīng)發(fā)生M1極化的KCs向M2表型偏移,考慮可能與huM SCs分泌細胞因子有關(guān),起到一種免疫調(diào)節(jié)作用,huM SCs調(diào)節(jié)巨噬細胞極化的分子機制可能與通過JAK-STAT信號轉(zhuǎn)導(dǎo)通路有關(guān)。
[Abstract]:Objective to induce the polarization change of Kupffer cells in Kupffer cells induced by lipopolysaccharide (LPS), and then co-culture KCs induced by LPS and human umbilical cord blood mesenchymal stem cells (HUMSCs) in Transwell. Methods the effects of huM SCs on KCs polarization shift were observed. Methods the supernatant factors, such as IL-4, TNF- 偽, IL-10, IL-6 and IL-6, were measured by ELISA method in KCs group (KCs LPS group). Inducible nitric oxide synthase (iNOS), argininase 1 (Arg-1), signal transduction and transcriptional activator (3) STAT-3 (STAT-6), and nuclear factor kappa B (NF- 魏 B) were detected by Western bolt. Results the secretion of proinflammatory factor TNF- 偽 and IL-6 in KCs LPS group was increased, while IL-10 and IL-4 secretion were increased in KCs LPS MSCs group, while Western blot test showed that iNOS increased NF- 魏 B p65 in KCs LPS group, which was also verified by real-time fluorescence quantitative PCRQRT-PCR.Results in KCs LPS group, the secretion of proinflammatory factor TNF- 偽 and IL-6 increased, while in KCs LPS MSCs group, the secretion of IL-10 and IL-4 was increased, while that in Western blot group was increased. In KCs LPS MSCs group, the expression of Arg-1 was highly expressed, and the expression of pS TAT-3pS TAT-6 was increased. Conclusion huM SCs can induce KCs with M1 polarization to M2 phenotypic shift, which may be related to the secretion of cytokines by huM SCs. The molecular mechanism of hum SCs regulating macrophage polarization may be related to JAK-STAT signal transduction pathway.
【作者單位】： 安徽醫(yī)科大學(xué)第三附屬醫(yī)院(合肥市第一人民醫(yī)院)消化內(nèi)科;安徽醫(yī)科大學(xué)公共衛(wèi)生學(xué)院;
【基金】：國家自然科學(xué)基金(編號:81101272)
【分類號】：R575

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