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实验性炎症和轴突切断术对猪降结肠壁内神经结构中亮氨酸脑啡肽(leuENK)分布的影响。

The influence of experimental inflammation and axotomy on leucine enkephalin (leuENK) distribution in intramural nervous structures of the porcine descending colon.

作者信息

Gonkowski Slawomir, Makowska Krystyna, Calka Jaroslaw

机构信息

Department of Clinical Physiology, Faculty of Veterinary Medicine, University of Warmia and Mazury, Oczapowski Str, 13, Olsztyn, Poland.

出版信息

BMC Vet Res. 2018 May 24;14(1):169. doi: 10.1186/s12917-018-1496-y.

DOI:10.1186/s12917-018-1496-y
PMID:29793486
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5968568/
Abstract

BACKGROUND

The enteric nervous system (ENS), located in the intestinal wall and characterized by considerable independence from the central nervous system, consists of millions of cells. Enteric neurons control the majority of functions of the gastrointestinal tract using a wide range of substances, which are neuromediators and/or neuromodulators. One of them is leucine-enkephalin (leuENK), which belongs to the endogenous opioid family. It is known that opioids in the gastrointestinal tract have various functions, including visceral pain conduction, intestinal motility and secretion and immune processes, but many aspects of distribution and function of leuENK in the ENS, especially during pathological states, remain unknown.

RESULTS

During this experiment, the distribution of leuENK - like immunoreactive (leuENK-LI) nervous structures using the immunofluorescence technique were studied in the porcine colon in physiological conditions, during chemically-induced inflammation and after axotomy. The study included the circular muscle layer, myenteric (MP), outer submucous (OSP) and inner submucous plexus (ISP) and the mucosal layer. In control animals, the number of leuENK-LI neurons amounted to 4.86 ± 0.17%, 2.86 ± 0.28% and 1.07 ± 0.08% in the MP, OSP and ISP, respectively. Generally, both pathological stimuli caused an increase in the number of detected leuENK-LI cells, but the intensity of the observed changes depended on the factor studied and part of the ENS. The percentage of leuENK-LI perikarya amounted to 11.48 ± 0.96%, 8.71 ± 0.13% and 9.40 ± 0.76% during colitis, and 6.90 ± 0.52% 8.46 ± 12% and 4.48 ± 0.44% after axotomy in MP, OSP and ISP, respectively. Both processes also resulted in an increase in the number of leuENK-LI nerves in the circular muscle layer, whereas changes were less visible in the mucosa during inflammation and axotomy did not change the number of leuENK-LI mucosal fibers.

CONCLUSIONS

LeuENK in the ENS takes part in intestinal regulatory processes not only in physiological conditions, but also under pathological factors. The observed changes are probably connected with the participation of leuENK in sensory and motor innervation and the neuroprotective effects of this substance. Differences in the number of leuENK-LI neurons during inflammation and after axotomy may suggest that the exact functions of leuENK probably depend on the type of pathological factor acting on the intestine.

摘要

背景

肠神经系统(ENS)位于肠壁内,其特点是相对独立于中枢神经系统,由数百万个细胞组成。肠神经元利用多种神经递质和/或神经调质来控制胃肠道的大部分功能。其中之一是亮氨酸脑啡肽(leuENK),它属于内源性阿片肽家族。已知胃肠道中的阿片类物质具有多种功能,包括内脏痛传导、肠道运动和分泌以及免疫过程,但leuENK在肠神经系统中的分布和功能的许多方面,尤其是在病理状态下,仍不清楚。

结果

在本实验中,采用免疫荧光技术研究了生理状态下、化学诱导炎症期间及轴突切断后猪结肠中亮氨酸脑啡肽样免疫反应性(leuENK-LI)神经结构的分布。研究包括环形肌层、肌间神经丛(MP)、外黏膜下神经丛(OSP)、内黏膜下神经丛(ISP)和黏膜层。在对照动物中,MP、OSP和ISP中leuENK-LI神经元的数量分别为4.86±0.17%、2.86±0.28%和1.07±0.08%。一般来说,两种病理刺激均导致检测到的leuENK-LI细胞数量增加,但观察到的变化强度取决于所研究的因素和肠神经系统的部位。在结肠炎期间,MP、OSP和ISP中leuENK-LI核周体的百分比分别为11.48±0.96%、[此处原文有误,应为8.71±0.13%]和9.40±0.76%;轴突切断后,分别为6.90±0.52%、8.46±1.2%和4.48±0.44%。这两个过程还导致环形肌层中leuENK-LI神经数量增加,而在炎症期间黏膜中的变化不太明显,轴突切断未改变leuENK-LI黏膜纤维的数量。

结论

肠神经系统中的亮氨酸脑啡肽不仅在生理条件下,而且在病理因素作用下都参与肠道调节过程。观察到的变化可能与亮氨酸脑啡肽参与感觉和运动神经支配以及该物质的神经保护作用有关。炎症期间和轴突切断后leuENK-LI神经元数量的差异可能表明,亮氨酸脑啡肽的确切功能可能取决于作用于肠道的病理因素类型。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d48/5968568/1fa5279ed3f8/12917_2018_1496_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d48/5968568/6673931852a9/12917_2018_1496_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d48/5968568/d0775e0d7198/12917_2018_1496_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d48/5968568/58f4cc851ff2/12917_2018_1496_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d48/5968568/146429688c51/12917_2018_1496_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d48/5968568/15102639fe8a/12917_2018_1496_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d48/5968568/1fa5279ed3f8/12917_2018_1496_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d48/5968568/6673931852a9/12917_2018_1496_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d48/5968568/d0775e0d7198/12917_2018_1496_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d48/5968568/58f4cc851ff2/12917_2018_1496_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d48/5968568/146429688c51/12917_2018_1496_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d48/5968568/15102639fe8a/12917_2018_1496_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d48/5968568/1fa5279ed3f8/12917_2018_1496_Fig6_HTML.jpg

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