| 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） |
|
| 摘要点击次数: 537 |
| 全文下载次数: 260 |
| 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. |
|
查看全文
查看/发表评论 下载PDF阅读器 |
| 关闭 |
