...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>World Journal of Gastroenterology >Effect of IL-4 on altered expression of complement activation regulators in rat pancreatic cells during severe acute pancreatitis.
【24h】

Effect of IL-4 on altered expression of complement activation regulators in rat pancreatic cells during severe acute pancreatitis.

机译：IL-4对重症急性胰腺炎大鼠胰腺细胞补体激活调节剂表达改变的影响。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

AIM: To investigate the effect of IL-4 on the altered expression of complement activation regulators in pancreas and pancreatic necrosis during experimental severe acute pancreatitis (SAP).METHODS: SAP model of rats was established by retrograde injection of 5% sodium taurocholate (1 mL/kg) into the pancreatic duct. We immunohistochemically assayed the expression of three complement activation regulators: decay accelerating factor (DAF; CD55), 20 ku homologous restriction factor (HRF20; CD59) and membrane cofactor protein (MCP; CD46), in the pancreatic acinar cells of rats at 0, 3, 6, 12, and 24 h after the induction of SAP model. Meanwhile the levels of amylase and lipase were determined, and morphological examination was performed. Then, 61 rats were randomly divided into three groups. Group A (n=21) received no treatment after the SAP model was established; group B (n=20) was given IL-4 (8 microg/animal) intraperitoneally 0.5 h before the SAP model was established; group C (n=20) was given IL-4 (8 microg/animal) intraperitoneally 0.5 h after the SAP model was established. Plasma amylase and lipase, extent of pancreatic necrosis and expression of complement activation regulators were investigated 6 h after the induction of SAP model.RESULTS: Three complement activation regulators were all expressed in pancreatic acinar cells. MCP was not found on the basolateral surface as reported. Contrary to the gradually increasing plasma level of amylase and lipase, expression of complement activation regulators decreased after SAP model was set up. At the same time, the severity of pancreatic necrosis was enhanced. A strong negative correlation was found between the expression of MCP, DAF, CD59 in pancreatic acinar cells and the severity of pancreatic necrosis (r= -0.748, -0.827, -0.723; P<0.01). In the second series of experiments, no matter when the treatment of IL-4 was given (before or after the induction of SAP model), the serum level of amylase or lipase was decreased and the extent of pancreatic necrosis was ameliorated significantly. Compared to SAP control group, the expression of DAF and CD59 in pancreas was reinforced when IL-4 was given before the induction of SAP model (P<0.01, P<0.05), but the expression of MCP was not influenced (P>0.05). The expression of DAF was enhanced, when IL-4 was given after the induction of SAP model (P<0.05), but the expression of CD59 and MCP did not change (P>0.05).CONCLUSION: Complement activation regulators may participate in the pathogenesis of pancreatic inflammation. Downregulation of complement activation regulators expression may be one of the causes of pancreatic necrosis. IL-4 treatment may control SAP aggravation by enhancing expression of DAF and CD59 in pancreas and decreasing pancreatic necrosis. Moreover, DAF and CD59 may play an important role in the regulation of complement activation regulators during SAP.
机译：目的：研究IL-4对实验性重症急性胰腺炎（SAP）大鼠胰腺和胰腺坏死中补体激活调节因子表达改变的影响。方法：通过逆行注射5％牛磺胆酸钠（1）建立大鼠SAP模型。 mL / kg）注入胰管。我们采用免疫组织化学方法检测了大鼠胰腺腺泡细胞中三种补体激活调节因子的表达：衰减加速因子（DAF; CD55），20 ku同源限制因子（HRF20; CD59）和膜辅因子蛋白（MCP; CD46），在0，引入SAP模型后的3、6、12和24小时。同时测定淀粉酶和脂肪酶的水平，并进行形态学检查。然后，将61只大鼠随机分为三组。建立SAP模型后，A组（n = 21）未接受任何治疗。 B组（n = 20）在建立SAP模型前0.5小时腹腔给予IL-4（8微克/动物）。建立SAP模型后，于C组（n = 20）腹膜内给予IL-4（8微克/动物）腹膜内注射。在SAP模型诱导6小时后，检测血浆淀粉酶和脂肪酶，胰腺坏死程度和补体激活调节剂的表达。结果：三种活化剂均在胰腺腺泡细胞中表达。据报道，在基底外侧表面未发现MCP。与血浆淀粉酶和脂肪酶水平逐渐升高相反，SAP模型建立后补体激活调节剂的表达下降。同时，胰腺坏死的严重程度增加了。胰腺腺泡细胞中MCP，DAF，CD59的表达与胰腺坏死的严重程度之间存在极强的负相关性（r = -0.748，-0.827，-0.723； P <0.01）。在第二系列实验中，无论何时给予IL-4治疗（在SAP模型诱导之前或之后），血清淀粉酶或脂肪酶水平均下降，胰腺坏死程度明显改善。与SAP对照组相比，诱导SAP模型前给予IL-4可增强胰腺DAF和CD59的表达（P <0.01，P <0.05），而MCP的表达不受影响（P> 0.05）。 ）。诱导SAP模型后给予IL-4时，DAF的表达增强（P <0.05），而CD59和MCP的表达不变（P> 0.05）。结论：补体激活调节剂可能参与了DAF的表达。胰腺炎症的发病机制。补体激活调节剂表达的下调可能是胰腺坏死的原因之一。 IL-4治疗可通过增强胰腺中DAF和CD59的表达并减少胰腺坏死来控制SAP恶化。此外，DAF和CD59可能在SAP期间对补体激活调节剂的调节中起重要作用。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号