| KD患儿血清对细胞活力及NF-κB表达的影响和PDTC的干预 |
| 投稿时间：2014-09-28 修订日期：2014-10-19 点此下载全文 |
| 引用本文：薛超超,李丰,仇慧仙,陈其,张园海.KD患儿血清对细胞活力及NF-κB表达的影响和PDTC的干预[J].医学研究杂志,2015,44(7):83-87 |
| DOI：
10.11969/j.issn.1673-548X.2015.07.024 |
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| 基金项目:浙江省医药卫生科技计划项目(201478482) |
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| 中文摘要:目的 研究川崎病(KD)患儿血清对人脐静脉内皮细胞(HUVEC)细胞活力及核转录因子-κB(NF-κB)表达的影响,探讨KD及其并发症的发病机制。观察吡咯烷二硫氨基甲酸酯(PDTC)干预下HUVEC细胞活力及NF-κB表达的变化,探讨PDTC的作用机制和潜在的临床应用价值。方法 根据不同的干预方法将培养的细胞分成4组:N组:RPMI1640培养基+正常儿童血清,K组:RPMI1640培养基+KD患儿血清,G组:RPMI1640培养基+KD患儿血清+IVIG;P组:RPMI1640培养基+KD患儿血清+PDTC。细胞培养24h后,MTT法检测细胞活力,RT-PCR法检测细胞内NF-κB p65mRNA的表达,Western blot法检测细胞核内NF-κB p65蛋白的合成。结果 K组HUVEC增殖受限,细胞活力较N组显著下降(P<0.05),NF-κB p65mRNA、NF-κB p65蛋白表达较N组显著升高(P<0.05); G组与P组细胞活力较K组显著增强(P<0.05),NF-κB p65mRNA、NF-κB p65蛋白表达均较K组显著降低。结论 KD患儿血清能促使细胞内NF-κB信号通路过度激活,导致细胞自身损伤,推测与KD的发生、发展密切相关。PDTC能有效抑制细胞内NF-κB信号通路,对细胞起保护作用,在KD的治疗上有潜在的临床价值。 |
| 中文关键词:川崎病 核因子 人脐静脉内皮细胞 吡咯烷二硫氨基甲酸酯 |
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| Effects of Serum from KD Patients on HUVEC viability and Expression of NF-κB and the Intervention of PDTC |
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| Abstract:Objective To investigate the influence on the viability of human umbilical vein endothelial cell (HUVEC) and its expression of NF-κB stimulated by serum from Kawasaki disease (KD) patients, and discuss the possible pathogenesis of KD and its complications.To observe the intervention effect of Pyrrolidine dithiocarbamate (PDTC) on the cell viability and the expression of NF-κB to explore its mechanism and potential clinical value. Methods HUVECs were divided into 4 groups,and each group was given different interfere respectively as following: Group N(RPMI-1640 medium+ normal serum); Group K(RPMI-1640 medium+ KD serum); Group G(RPMI-1640 medium+ KD serum+ IVIG); Group P(RPMI-1640 medium+ KD serum+ PDTC). The cells in each group were cultured for 24 hours before cell viabilities were tested by MTT. The expressions of NF-κB p65mRNA were measured by RT-PCR and the expressions of the NF-κB p65 protein by Western blot. Results The cell growth in Group K was inhibited,and its viability was significantly lower than that in Group N (P<0.05). The expressions of NF-κB p65mRNA and NF-κB p65 protein in Group K were both significantly higher than that in Group N (P<0.05). The viabilities of cells in Group G and P both increased significantly than those in Group K (P<0.05). The expressions of NF-κB p65mRNA and NF-κB p65 protein in Group G and P were all much lower than those in Group K (P<0.05). Conclusion KD serum can make NF-κB signaling pathway excessive express and lead to cell-self lesion, which may play an important role on the pathogenesis of KD.PDTC can effectively inhibit NF-κB signaling pathway excessive expression and protect the cell, which indicates it has potential clinical value for KD. |
| keywords:Kawasaki disease NF-κB HUVEC PDTC |
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