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作 者:李旺林[1] 曹杰[1] 兰平[2] 杨平[1] 钟俊斌[1] 杨建荣[1] 张通[1] 王强[1]
机构地区:[1]广州医学院附属广州市第一人民医院胃肠外科,510180 [2]中山大学附属第六医院结直肠肛门外科
出 处:《中华胃肠外科杂志》2013年第4期386-389,共4页Chinese Journal of Gastrointestinal Surgery
基 金:广州医学院科学研究项目(2010C19);广东省科技计划项目[(2011)177-1];广州市医药卫生科技项目(20121A011018)
摘 要:目的研究旋毛虫T.spiralis感染对小鼠结肠黏膜表皮钙黏附素(E—cadherin)的影响及其作用机制。方法选择BALB/c小鼠和STAT6基因敲除(Th2缺乏)的STAT6-/-小鼠,分为T.spiralis感染组和无感染的对照组,每组中BALB/c小鼠和STAT6-/-小鼠各5只。感染7d后直肠灌注辣根过氧化物酶(HRP),灌注后0、60和120min分析小鼠血液中HRP水平以检测结肠通透性;随后处死小鼠,取小鼠结肠,免疫荧光染色观察小鼠结肠黏膜中E—cadherin的分布,Westernblot检测小鼠结肠黏膜中E—cadherin的表达,ELISA法检测肠系膜淋巴结中IL.4的表达。结果感染组BALB/c小鼠血清HRP水平较对照组显著增高(P〈0.05):而STAT6-/-小鼠感染组与对照组血清血清HRP水平差异无统计学意义(尸〉0.05)。BALB/c小鼠感染组结肠上皮细胞中E.cadherin均位于细胞质,而在对照组中位于细胞膜;同时,感染组E.cadherin表达水平明显较对照组降低。而STAT6-/-小鼠感染组与对照组中E.cadherin的分布和表达均无明显变化。BALB/c小鼠感染组肠系膜淋巴结IL。4水平为(193.0±12.5)ng/ml。明显高于BALB/c小鼠对照组和STAT6-/-小鼠感染组[(21.0±2.3)ng/ml和(15.0±3.1)ng/ml;均P〈0.05]。结论T.spiralis感染能够导致小鼠结肠上皮E—cadherin分布和表达的改变,其作用机制可能是通过诱导Th2的分泌来实现。[Abstract] Objective To study the effect of Trichinella spiralis (T.spiralis) infection on the expression and distribution of colonic epithelial E-cadherin in mice and its mechanism. Methods BALB/c mice and STAT6-/- mice were infected with T.spiralis, and mice without infection were used as control. Seven days later, the horseradish peroxidase (HRP) was infused by rectal enema. Serum HRP was detected in the subsequent 0, 60 and 120 minutes. Then the mice were sacrificed and colon was taken out. The distribution of E-cadherin in colon was detected by staining, and the expression of E-cadherin was detected by Western blot. The expression of interleukin-4 (IL-4) in mesenteric lymph nodes was detected by ELISA. Results Serum HRP level in infected BALB/c mice was significantly higher than that in control mice (P〈0.05), while it was not significantly different between infected STAT6-/- mice and controls (P〉0.05). In infected BALB/c mice, E-cadherin located in cytoplasm of colonic epithelial cells, while in controls, it located in cellular membrane. E-caherin expression down-regulated significantly in infected BALB/c mice as compared to controls. E-cadherin expression and distribution did not change obviously in infected STAT6-/- and control mice. IL-4 level in mesenteric lymph nodes of infected BALB/c mice[ (193.0±12.5)ug/L] was significantly higher as compared to control BALB/c and infected STAT6-/- mice[(21.O±2.3) Ixg/L and(15.0±3.1) I.Lg/L, all P〈0.05]. Conclusion T.spiralis infection can increase colonic epithelial permeability of mice, which may be associated with induction of Th2 cytokine secretion.
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