细胞焦亡在新生儿坏死性小肠结肠炎中的致病作用
发布时间:2018-06-09 03:32
本文选题:细胞焦亡 + 坏死性小肠结肠炎 ; 参考:《第三军医大学学报》2017年14期
【摘要】:目的探讨细胞焦亡是否参与新生儿坏死性小肠结肠炎(necrotizing enterocolitis,NEC)发病,并分析其可能的作用机制。方法将50只新生1 d的SD大鼠按随机数字表法分为2组(n=25):正常对照组、坏死性小肠结肠炎新生大鼠组(NEC组)。正常对照组与母鼠同笼,不予处理;NEC组采用缺氧、冷刺激及人工喂养的方式建立模型。新生鼠于第1、2、3天固定时间点测量体质量,第4天处死大鼠,HE染色观察回盲部肠组织病理学变化并评分;qPCR检测NLRP3、IL-1β、IL-18基因表达水平;Western blot检测Caspase-1表达及激活情况;ELISA检测肠组织匀浆IL-1β、IL-18水平。结果与正常对照组相比,NEC组大鼠体质量明显降低,肠上皮损伤明显;NLRP3及IL-1β、IL-18基因表达增高(分别为0.33±0.06 vs 1.11±0.12,0.40±0.15 vs 1.25±0.13,1.04±0.16 vs 2.35±0.17,P0.05);激活的Caspase-1仅在NEC组中表达,且下游炎症因子IL-1β及IL-18水平亦高于正常对照组(分别为300.4±76.5 vs 74.4±17.5,214.4±28.1 vs 23.9±19.3,P0.01)。结论细胞焦亡参与了NEC的发病,其具体机制可能与焦亡发生后IL-1β、IL-18的水平升高有关。
[Abstract]:Objective to investigate the role of cellular pyrolysis in the pathogenesis of neonatal necrotizing enterocolitis (NEC) and to analyze its possible mechanism. Methods Fifty Sprague-Dawley rats were randomly divided into two groups: normal control group, NEC group and NEC group. The NEC group was treated with hypoxia, cold stimulation and artificial feeding. The body mass of newborn rats was measured at a fixed time point of 3 days on the 1st day. On the 4th day, the rats were killed to observe the histopathological changes of ileocecal intestinal tissue by HE staining and to evaluate the expression level of IL-18 gene in the ileocecal intestine by qPCR. The expression and activation of Caspase-1 in intestinal homogenate were detected by Western blot and the level of IL-18 in intestinal homogenate was detected by enzyme-linked immunosorbent assay (Elisa). Results compared with the normal control group, the body mass of rats in NEC group was significantly lower, and the expression of NLRP3 and IL-1 尾 IL-18 in intestinal epithelial injury was significantly increased (0.33 卤0.06 vs 1.11 卤0.120.40 卤0.15 vs 1.25 卤0.131.04 卤0.16 vs 2.35 卤0.17P0.05respectively), and the expression of activated Caspase-1 was found only in NEC group. The levels of IL-1 尾 and IL-18 were also higher than those in the normal control group (300.4 卤76.5 vs 74.4 卤17.5214.4 卤28.1 vs 23.9 卤19.3P 0.01, respectively). Conclusion the pathogenesis of NEC may be related to the increase of IL-1 尾 -IL-18 level.
【作者单位】: 重庆医科大学附属儿童医院新生儿科儿童发育疾病研究教育部重点实验室儿科学重庆市重点实验室儿童发育重大疾病国家国际科技合作基地;
【基金】:国家自然科学基金(81370744,81571483,81601323) 儿童医院临床研究项目[(2014)254-lcyj2014-11]~~
【分类号】:R722.1
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本文编号:1998682
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