倪建波,胡国勇,万 荣,王兴鹏.白介素-17A在小鼠慢性胰腺炎中的作用研究[J].,2017,17(5):801-805 |
白介素-17A在小鼠慢性胰腺炎中的作用研究 |
Involvement of Interleukin-17A in Caerulein-induced Chronic Pancreatitis in Mice |
投稿时间:2016-08-27 修订日期:2016-09-15 |
DOI:10.13241/j.cnki.pmb.2017.05.001 |
中文关键词: 白介素-17A 慢性胰腺炎 胰腺星状细胞 胰腺纤维化 |
英文关键词: Interleukin-17A Chronic pancreatitis Pancreatic stellate cell Pancreatic fibrosis |
基金项目:国家自然科学基金青年科学基金项目(81400663);国家自然科学基金面上项目(81400663) |
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中文摘要: |
摘要 目的:研究白细胞介素-17A在小鼠慢性胰腺炎模型中的表达及其对小鼠星状细胞的影响。方法:建立雨蛙肽诱导的小鼠实验性慢性胰腺炎动物模型,利用实时荧光定量PCR、ELISA、免疫组化和Western-blot等手段检测白介素-17A在雨蛙肽诱导的小鼠慢性胰腺炎模型中的表达变化及免疫活性。用重组白介素-17A作用于小鼠胰腺星状细胞,检测其对星状细胞活化的作用,并进一步探究其对促胰腺纤维化炎症因子白介素-6、白介素-1β、TGF-β在mRNA水平的表达变化。结果:慢性胰腺炎胰腺组织中白介素-17A受体IL-17RA及IL-17RC mRNA水平的表达较正常胰腺明显升高,慢性胰腺炎小鼠胰腺组织中IL-17A蛋白水平较正常小鼠明显升高,CP小鼠血清中IL-17A蛋白水平(56.40±10.50 pg/L)较NC组(27.88±5.74pg/L)亦明显升高,IL-17A在正常胰腺组织中鲜有表达(8.9±2.72%),而在CP组织中呈强阳性表达(55.84±5.71%),其免疫活性主要定位于间质炎性细胞及导管样复合体中;重组白介素-17A可促进小鼠星状细胞活化,并直接诱导星状细胞表达白介素-6、白介素-1β以及TGF-β等促纤维化细胞因子。结论:白介素-17A在雨蛙肽诱导的小鼠慢性胰腺炎模型中表达上调,并可能通过诱导小鼠星状细胞表达促炎细胞因子白介素-6、白介素-1β和TGF-β,促进胰腺星状细胞活化以及胰腺纤维化。 |
英文摘要: |
ABSTRACT Objective: Interleukin (IL)-17A palys an vital role in various in ammatory diseases such as chronic inflammation and autoimmune diseases including autoimmune pancreatitis, but the role of IL-17A in chronic pancreatitis has not been clarified. This study aimed to study the role of IL-17A in experimental chronic pancreatitis (CP) induced by caerulein in mice. Methods: We firstly examined the expression levels of IL-17A during caerulein-induced CP in vivo in mice by qRT-PCR, Western blotting, ELISA, and immunoreactiv- ity by immunohistochemistry. The effects of IL-17A on pancreatic stellate cells (PSCs) were further investigated in vitro using recombi- nant IL-17A (rIL-17A). Results: Expression of IL-17RA and IL-17RC mRNAs were remarkably upregulated during CP, IL-17A protein level in pancreatic tissues was increased aftrer stimulation with caerulein, the serum concentration of IL-17A was also significantly ele- vated in CP mice (56.40±10.50 pg/L) compared with NC group (27.88±5.74pg/L). Immunoreactivity of IL-17A was rarely examined in normal pancreatic tissue (8.9±2.72%), but the positive cells were remarkebly increased in CP mice (55.84±5.71%), which were mainly localized in interstitial inflammatory cells and tubular complexes. Futhermore, rIL-17A promoted activation of pancreatic stellate cell in vitro, and directly stimulated expression of several profibrotic genes, including IL-6, IL-1β and TGF-β in PSCs. Conclusion: IL-17A plays a role in activating PSCs by inducing the expression of Chronic pancreatitis mediators, and probably promote pancreatic fibrosis during experimental chronic pancreatitis. |
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