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人脱落乳牙干细胞通过抑制内质网应激减轻大鼠三叉神经痛。

Stem cells from human exfoliated deciduous teeth attenuate trigeminal neuralgia in rats by inhibiting endoplasmic reticulum stress.

作者信息

Yang Zhijie, Wang Chun, Zhang Xia, Li Jing, Zhang Ziqi, Tan Zhao, Wang Junyi, Zhang Junyang, Bai Xiaofeng

机构信息

Department of Oral and Maxillofacial Surgery, Hospital of Stomatology, China Medical University, Shenyang, China.

Liaoning Provincial Key Laboratory of Oral Diseases, Shenyang, China.

出版信息

Korean J Pain. 2022 Oct 1;35(4):383-390. doi: 10.3344/kjp.2022.35.4.383.

DOI:10.3344/kjp.2022.35.4.383
PMID:36175337
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9530689/
Abstract

BACKGROUND

The treatment of trigeminal neuralgia remains a challenging issue. Stem cells from human exfoliated deciduous teeth (SHED) provide optimized therapy for chronic pain. This study aimed to investigate the mechanisms underlying the attenuation of trigeminal neuralgia by SHED.

METHODS

Trigeminal neuralgia was induced by chronic constriction injury of the infraorbital nerve. The mechanical threshold was assessed after model establishment and local SHED transplantation. Endoplasmic reticulum (ER) morphology and Caspase12 expression in trigeminal ganglion (TG) was evaluated as well. BiP expression was observed in PC12 cells induced by tunicamycin.

RESULTS

The local transplantation of SHED could relieve trigeminal neuralgia in rats. Further, transmission electron microscopy revealed swelling of the ER in rats with trigeminal neuralgia. Moreover, SHED inhibited the tunicamycin-induced up-regulated expression of BiP mRNA and protein in vitro. Additionally, SHED decreased the up-regulated expression of Caspase12 mRNA and protein in the TG of rats caused by trigeminal neuralgia after chronic constriction injury of the infraorbital nerve mode.

CONCLUSIONS

This findings demonstrated that SHED could alleviate pain by relieving ER stress which provide potential basic evidence for clinical pain treatment.

摘要

背景

三叉神经痛的治疗仍然是一个具有挑战性的问题。人脱落乳牙干细胞(SHED)为慢性疼痛提供了优化的治疗方法。本研究旨在探讨SHED减轻三叉神经痛的潜在机制。

方法

通过眶下神经慢性压迫损伤诱导三叉神经痛。在模型建立和局部SHED移植后评估机械阈值。还评估了三叉神经节(TG)中的内质网(ER)形态和半胱天冬酶12的表达。观察了衣霉素诱导的PC12细胞中结合免疫球蛋白蛋白(BiP)的表达。

结果

局部移植SHED可缓解大鼠三叉神经痛。此外,透射电子显微镜显示三叉神经痛大鼠的内质网肿胀。此外,SHED在体外抑制了衣霉素诱导的BiP mRNA和蛋白表达上调。此外,在眶下神经慢性压迫损伤模型导致三叉神经痛的大鼠TG中,SHED降低了半胱天冬酶12 mRNA和蛋白的上调表达。

结论

这些发现表明,SHED可通过减轻内质网应激来缓解疼痛,这为临床疼痛治疗提供了潜在的基础证据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7ff/9530689/3cd07a73aae0/kjp-35-4-383-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7ff/9530689/872a0778e07f/kjp-35-4-383-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7ff/9530689/cbcda4f88f08/kjp-35-4-383-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7ff/9530689/f15fbd92c682/kjp-35-4-383-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7ff/9530689/3cd07a73aae0/kjp-35-4-383-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7ff/9530689/872a0778e07f/kjp-35-4-383-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7ff/9530689/cbcda4f88f08/kjp-35-4-383-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7ff/9530689/f15fbd92c682/kjp-35-4-383-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7ff/9530689/3cd07a73aae0/kjp-35-4-383-f4.jpg

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