本文選題：細(xì)胞焦亡 + 壞死性小腸結(jié)腸炎��； 參考：《第三軍醫(yī)大學(xué)學(xué)報(bào)》2017年14期

【摘要】：目的探討細(xì)胞焦亡是否參與新生兒壞死性小腸結(jié)腸炎(necrotizing enterocolitis,NEC)發(fā)病,并分析其可能的作用機(jī)制。方法將50只新生1 d的SD大鼠按隨機(jī)數(shù)字表法分為2組(n=25):正常對(duì)照組、壞死性小腸結(jié)腸炎新生大鼠組(NEC組)。正常對(duì)照組與母鼠同籠,不予處理;NEC組采用缺氧、冷刺激及人工喂養(yǎng)的方式建立模型。新生鼠于第1、2、3天固定時(shí)間點(diǎn)測量體質(zhì)量,第4天處死大鼠,HE染色觀察回盲部腸組織病理學(xué)變化并評(píng)分;qPCR檢測NLRP3、IL-1β、IL-18基因表達(dá)水平;Western blot檢測Caspase-1表達(dá)及激活情況;ELISA檢測腸組織勻漿IL-1β、IL-18水平。結(jié)果與正常對(duì)照組相比,NEC組大鼠體質(zhì)量明顯降低,腸上皮損傷明顯;NLRP3及IL-1β、IL-18基因表達(dá)增高(分別為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僅在NEC組中表達(dá),且下游炎癥因子IL-1β及IL-18水平亦高于正常對(duì)照組(分別為300.4±76.5 vs 74.4±17.5,214.4±28.1 vs 23.9±19.3,P0.01)。結(jié)論細(xì)胞焦亡參與了NEC的發(fā)病,其具體機(jī)制可能與焦亡發(fā)生后IL-1β、IL-18的水平升高有關(guān)。
[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 鹵0.06 vs 1.11 鹵0.120.40 鹵0.15 vs 1.25 鹵0.131.04 鹵0.16 vs 2.35 鹵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 鹵76.5 vs 74.4 鹵17.5214.4 鹵28.1 vs 23.9 鹵19.3P 0.01, respectively). Conclusion the pathogenesis of NEC may be related to the increase of IL-1 尾 -IL-18 level.
【作者單位】： 重慶醫(yī)科大學(xué)附屬兒童醫(yī)院新生兒科兒童發(fā)育疾病研究教育部重點(diǎn)實(shí)驗(yàn)室兒科學(xué)重慶市重點(diǎn)實(shí)驗(yàn)室兒童發(fā)育重大疾病國家國際科技合作基地;
【基金】：國家自然科學(xué)基金(81370744,81571483,81601323) 兒童醫(yī)院臨床研究項(xiàng)目[(2014)254-lcyj2014-11]~~
【分類號(hào)】：R722.1
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本文編號(hào)：1998682