...
首页> 外文期刊>Neurogastroenterology and motility >Electroacupuncture promotes the gastrointestinal motility of diabetic mice by CNP/NPR‐B‐cGMP and PDE3A‐cGMP signaling
【24h】

Electroacupuncture promotes the gastrointestinal motility of diabetic mice by CNP/NPR‐B‐cGMP and PDE3A‐cGMP signaling

机译:通过CNP / NPR-B-CGMP和PDE3A-CGMP信号传导促进糖尿病小鼠的胃肠胃动力促进

获取原文
获取原文并翻译 | 示例
   

获取外文期刊封面封底 >>

       

摘要

Abstract Background Electroacupuncture (EA) can promote gastrointestinal (GI) motility of diabetic mice, but the mechanism is not clearly elucidated. Natriuretic peptides (NPs) were related to the diabetes‐induced gut dysfunction of mice, which may be associated with ICC (interstitial cells of cajal). Besides, EA could increase the ICC of diabetic mice. Our aim was to explore whether EA can promote the gut motility by CNP/NPR‐B‐cGMP and PDE3A‐cGMP signaling in diabetic mice, and the relationship between NPs and ICC. Methods Wild C57BL/6 male mice were divided into five groups: control group, diabetic mellitus (DM group), diabetic mellitus plus sham EA group (SEA), diabetic mellitus plus low‐frequency EA group (LEA), and diabetic mellitus plus high‐frequency group (HEA). Gastrointestinal motility was assessed by gastric emptying and GI transit test. Immunofluorescence staining was applied to assess the expression level of CNP, NPR‐B, and c‐Kit. Western blot, PCR, and ELISA were used to detect the level of CNP, NPR‐B, PDE2A, PDE3A, c‐Kit, mSCF, and cGMP content. The correlativity between NPR‐B and mSCF was evaluated by Pearson's correlation and linear regression analyses. Key Results (a) EA could improve the GI dysfunction of diabetic mice. (b) CNP, NPR‐B, and cGMP contents were decreased, but the level of PDE3A, c‐Kit, and mSCF was increased in the EA groups. (c) There was a negative correlation between NPR‐B and mSCF among the groups. Conclusions and Inferences Electroacupuncture promotes the GI function by CNP/NPR‐B‐cGMP and PDE3A‐cGMP signaling in diabetic mice; up‐regulated mSCF/c‐Kit signaling by EA may be mediated partially via down‐regulation of CNP/NPR‐B signaling.
机译:摘要背景电针(EA)可以促进糖尿病小鼠的胃肠道(GI)运动,但没有明确阐明机制。利钠肽(NPS)与小鼠的糖尿病诱导的肠道功能障碍有关,其可能与ICC(CAGAL的间质细胞)相关。此外,EA可以增加糖尿病小鼠的ICC。我们的目的是探索EA是否可以通过CNP / NPR-B-CGMP和PDE3A-CGMP信号传导在糖尿病小鼠中促进肠蠕动,以及NPS和ICC之间的关系。方法将野生C57BL / 6雄性小鼠分为五组:对照组,糖尿病患者(DM组),糖尿病MELLITUS加假EA组(SEA),糖尿病MELLITUS加低频EA组(LEA),糖尿病患者和糖尿病 - 频率组(HEA)。通过胃排空和GI转运试验评估胃肠动力。应用免疫荧光染色以评估CNP,NPR-B和C-kit的表达水平。用于检测CNP,NPR-B,PDE2A,PDE3A,C-KIT,MSCF和CGMP含量的水平。通过Pearson的相关性和线性回归分析评估了NPR-B和MSCF之间的相关性。关键结果(a)EA可以改善糖尿病小鼠的GI功能障碍。 (b)CNP,NPR-B和CGMP含量降低,但在EA组中增加了PDE3A,C-kit和MSCF的水平。 (c)组中NPR-B和MSCF之间存在负相关性。结论和推迟电针通过CNP / NPR-B-CGMP和PDE3A-CGMP信号传导在糖尿病小鼠中促进GI功能;通过EA可以通过CNP / NPR-B信号的下调部分地介导上调的MSCF / C-kit信号。

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