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电针对糖尿病性便秘大鼠结肠平滑肌 Cajal 间质细胞凋亡/增殖的调节作用及其对结肠运动的恢复作用。

Electroacupuncture regulates apoptosis/proliferation of intramuscular interstitial cells of cajal and restores colonic motility in diabetic constipation rats.

机构信息

Division of Gastroenterology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1277 Jiefang Road, Wuhan, Hubei 430022, China.

出版信息

Evid Based Complement Alternat Med. 2013;2013:584179. doi: 10.1155/2013/584179. Epub 2013 Nov 18.

DOI:10.1155/2013/584179
PMID:24348706
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3852313/
Abstract

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.

摘要

Cajal 间质细胞（ICC）的损伤与糖尿病大鼠的肠道动力障碍有关。我们已经证明电针刺激（EAS）可以加速结肠收缩。然而，对于 EAS 对结肠通过性和 ICC 的潜在作用知之甚少。在这项研究中，我们评估了 EAS 对结肠通过性的影响，并研究了 ICC 的凋亡/增殖是否参与了 EAS 对结肠通过性的调节作用。大鼠被随机分为正常、糖尿病、糖尿病加假刺激、糖尿病加低频刺激和糖尿病加高频刺激组。采用珠排出试验测量远端结肠通过性。通过 Western blot 检测 Kit（ICC 标志物）。通过末端 dUTP 核苷酸末端标记法检测凋亡 ICC。通过 Kit/Ki67 双重免疫荧光染色对全层标本检测增殖 ICC。使用电子显微镜研究 ICC 的超微结构变化。结果表明，高频刺激显著促进了结肠通过性。低和高频刺激明显挽救了肌间 ICC 的凋亡。在低和高频刺激组中发现了丰富的增殖肌间 ICC。我们的结果表明，高频 EAS 对远端结肠通过性具有刺激作用，这可能是通过下调肌间 ICC 的凋亡和上调增殖来介导的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc87/3852313/b4d557dc16fb/ECAM2013-584179.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc87/3852313/6a41ab84f57f/ECAM2013-584179.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc87/3852313/64c58360d6ec/ECAM2013-584179.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc87/3852313/11479d056268/ECAM2013-584179.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc87/3852313/1b87d076a33a/ECAM2013-584179.004.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc87/3852313/b4d557dc16fb/ECAM2013-584179.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc87/3852313/6a41ab84f57f/ECAM2013-584179.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc87/3852313/64c58360d6ec/ECAM2013-584179.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc87/3852313/11479d056268/ECAM2013-584179.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc87/3852313/1b87d076a33a/ECAM2013-584179.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc87/3852313/d1639ba5a6fb/ECAM2013-584179.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc87/3852313/b4d557dc16fb/ECAM2013-584179.006.jpg

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