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IL-33在肺纤维化小鼠的表达 被引量:4

Expression of IL-33 in mice with pulmonary fibrosis
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摘要 目的探讨IL-33在肺纤维化模型小鼠的表达。方法小鼠气管内一次性注入博来霉素制备急性肺纤维化模型(BLM组,20只),气管内注入等容积生理盐水作为对照(对照组,20只)。HE染色观察肺部炎症程度,Masson三色染色法检测纤维化程度。TUNEL细胞凋亡试剂盒检测肺上皮细胞凋亡,免疫组化法及Western blot检测IL-33、α-平滑肌肌动蛋白(α-SMA)和上皮型钙粘蛋白(E-cad)的动态表达。结果与对照组比较,在肺纤维化过程中,BLM组E-cad的表达量在第14、28天均明显下降,IL-33的表达在第3、7、14天明显增加,α-SMA的表达在第3、7、14、28天明显升高(P<0.05)。TUNEL显示BLM组在第7天凋亡细胞最多。结论肺纤维化过程中存在上皮细胞过度凋亡及成纤维细胞增殖失控,同时伴有IL-33的动态表达。 Objective To explore the expression of IL-33 in mice with pulmonary fibrosis.Methods Fourty mice were equally assigned into two groups.An acute pulmonary fibrosis model in group A was established by endotracheal bloemycin challenge once.The mice in group B were given normal saline as the controls.HE staining was performed to evaluate pulmonary inflammation.Masson′s trichrome was used to detect collagen.TUNEL apoptosis assay kit was used to detect epithelial apoptosis.Western blot and immunohistochemical analysis were adopted to detect the expressions of IL-33,E-cadherin and α-smooth muscle actin(α-SMA).Results Compared to group B,in group A,the expression of E-cadherin was lower on the 14thand 28th day(P0.05),the expression of α-SMA was higher on the 3rd,7th,14th and 28th day(P0.05),and the expression of IL-33 was higher on the 3rd,7th and 14th day(P0.05).The cell apoptosis in group A peaked on the 7th day.Conclusion The abnormal apoptosis of epithelial and proliferation of fibroblasts occur during the development of pulmonary fibrosis,which is accompanied by dynamic expression of IL-33.
出处 《江苏医药》 CAS 北大核心 2013年第4期373-375,F0003,共4页 Jiangsu Medical Journal
基金 卫生部科研项目(WKJ2006-2-026) 上海市自然科学基金项目(10ZR1422600)
关键词 白细胞介素33 肺纤维化 Interleukin-33 Pulmonary fibrosis
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  • 1Blom L, Poulsen LK. IL-1 family members IL-18 and IL-33 up-regulate the inflammatory potential of differentiated human Thl andTh2 cultures. J Immunol, 2012,189 (9) :43314337.
  • 2Yin H,Li XY,Jin XB,et al. IL-33 prolongs murine cardiac al-lograft survival through induction of TH2-type immune deviation.Transplantation, 2010,89( 10) : 1189-1197.
  • 3Talabot-Ayer D, Lamacchia C, Gabay C, et al. Interleukin-33 isbiologically active independent of caspase-1 cleavage. J BiolChem, 2009,284(29) : 19420-19426.
  • 4Sponheim J, Pollheimer J, Olsen T, et al. Inflammatory boweldisease-associated interleukin-33 is preferentially expressed in ul-ceration-associated myofibroblasts. Am J Pathol, 2010,177(6):2804-2815.
  • 5Moussion C, Ortega N,Girard JP. The IL-1-like cytokine IL-33 isconstitutively expressed in the nucleus of endothelial cells and epi-thelial cells in vivo : a novel ‘ alarmin ’. PLoS One,2008,3(10):e3331.
  • 6Seltmann J, Werfel T, Wittmann M. Evidence for a regulatoryloop between IFN-7 and IL-33 in skin inflammation. Exp Derma-tol, 2013,22(2) :102-107.
  • 7Rankin AL, Mumm JB, Murphy E, et al. IL-33 induces IL-33-dependent cutaneous fibrosis. J Immunol, 2010,184(3) :1526-1535.
  • 8Cevikbas F, Steinhoff M. IL-33 : a novel danger signal system inatopic dermatitis. J Investig Med, 2012,60(B) :1151-1156.
  • 9Hueber AJ, Alves-Filho JC, Asquith DL,et al. IL-33 inducesskin inflammation with mast cell and neutrophil activation. Eur JImmunol, 2011, 41(8) :2229-2237.
  • 10Tajima S,Bando M,Ohno S,et al. ST2 gene induced by type 2helper T cell and proinflammatory cytokine stimuli may modulatelung injury and fibrosis. Exp Lung Res, 2007 , 33(2) :81-97.

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