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首页> 外文期刊>Evidence-based complementary and alternative medicine: eCAM >Electroacupuncture Regulates Apoptosis/Proliferation of Intramuscular Interstitial Cells of Cajal and Restores Colonic Motility in Diabetic Constipation Rats
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Electroacupuncture Regulates Apoptosis/Proliferation of Intramuscular Interstitial Cells of Cajal and Restores Colonic Motility in Diabetic Constipation Rats

机译:电针调节Cajal肌内间质细胞的凋亡/增殖,恢复糖尿病便秘大鼠的结肠运动

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摘要

Injury of interstitial cells of Cajal (ICC) is associated with gut dysmotility in diabetic rats. We have shown an acceleration of the colonic contractility by electroacupuncture stimulation (EAS). However, little is known about potential roles of EAS on colonic transit and ICC. In this study, we evaluate the effect of EAS on colonic transit and investigate whether apoptosis/proliferation of ICC was involved in regulative effect of EAS on colonic transit. Rats were randomly assigned to normal, diabetic, diabetic-plus-sham stimulation, diabetic-plus-low-frequency stimulation, and diabetic-plus-high-frequency stimulation groups. Bead expulsion test was used for measuring the distal colonic transit. The Kit (ICC marker) was detected by western blot. Apoptotic ICC was detected by terminal dUTP nucleotide end labeling. Proliferating ICC was identified by Kit/Ki67 double immunofluorescent staining on whole mount preparations. Ultrastructure changes of ICC were studied using electron microscopy. Results showed that high-frequency stimulation significantly promoted colonic transit. Low- and high-frequency stimulation markedly rescued intramuscular ICC from apoptosis. Abundant proliferating intramuscular ICC was found in low- and high-frequency stimulation groups. Our results indicate that high-frequency EAS has stimulatory effect on the distal colonic transit, which may be mediated by downregulation of the apoptosis and upregulation of the proliferation of intramuscular ICC.
机译:CAJAL(ICC)的间质细胞损伤与糖尿病大鼠的肠道功能性有关。我们通过电针刺激(EA)显示了对结肠收缩性的加速度。然而,很少有关于Sea在结肠过境和ICC上的潜在角色。在这项研究中,我们评估了EAS对结肠过境的影响,并研究了ICC的凋亡/扩散是否参与了SEA对结肠过境的调节作用。将大鼠随机分配到正常,糖尿病,糖尿病和假刺激,糖尿病 - 加低频刺激和糖尿病加 - 高频刺激组。珠子驱逐试验用于测量远端结肠转运。 KIT(ICC标记)被蛋白质印迹检测到。通过终末DUTP核苷酸末端标记检测凋亡ICC。通过KIT / KI67双免疫荧光染色在全架制剂上鉴定增殖ICC。使用电子显微镜研究ICC的超微结构变化。结果表明,高频刺激显着促进了结肠过境。低频和高频刺激显着拯救了肌肉内的ICC免受凋亡。在低频刺激组中发现丰富的增殖肌肉ICC。我们的结果表明,高频eas对远端结肠转运具有刺激性作用,该转运可能通过下调凋亡和肌肉内ICC的增殖的下调和上调。

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