Jiawei Fu , Chunshuai Wu , Guanhua Xu , Jinlong Zhang , Jiajia Chen , Chu Chen , Hongxiang Hong , Pengfei Xue , Jiawei Jiang , Jiayi Huang , Chunyan Ji , Zhiming Cui
{"title":"TNIP2对脊髓损伤后小胶质细胞炎症反应的保护作用","authors":"Jiawei Fu , Chunshuai Wu , Guanhua Xu , Jinlong Zhang , Jiajia Chen , Chu Chen , Hongxiang Hong , Pengfei Xue , Jiawei Jiang , Jiayi Huang , Chunyan Ji , Zhiming Cui","doi":"10.1016/j.npep.2023.102351","DOIUrl":null,"url":null,"abstract":"<div><h3>Background</h3><p>Spinal cord injury<span> (SCI) is a devastating disease that can lead to tissue loss and neurological dysfunction. TNIP2 is a negative regulator of NF-κB signaling due to its capacity to bind A20 and suppress inflammatory cytokines-induced NF-κB activation. However, the anti-inflammatory role of TNIP2 in SCI remains unclear. Our study's intention was to evaluate the effect of TNIP2 on the inflammatory response of microglia after spinal cord injury in rats.</span></p></div><div><h3>Methods</h3><p><span><span>HE </span>staining<span> and Nissl staining were performed on day 3 following SCI to analyze the histological changes. To further investigate the functional changes of TNIP2 after SCI, we performed immunofluorescence staining experiments. The effect of </span></span>LPS<span> on TNIP2 expression in BV2 cells was examined by western blot. The levels of TNF-α, IL-1β, and IL-6 in spinal cord tissues of rats with SCI and in BV2 cells with LPS were measured by using qPCR.</span></p></div><div><h3>Results</h3><p><span>TNIP2 expression was closely associated with the pathophysiology of SCI in rats, and TNIP2 was involved in regulating functional changes in microglia. TNIP2 expression was increased during SCI in rats and that overexpression of TNIP2 inhibited M1 polarization and pro-inflammatory cytokine production in microglia, which might ultimately protect against inflammatory responses through the </span>MAPK<span> and NF-κB signaling pathways.</span></p></div><div><h3>Conclusions</h3><p>The present study provides evidence for a role of TNIP2 in the regulation of inflammation in SCI and suggests that induction of TNIP2 expression alleviated the inflammatory response of microglia.</p></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"101 ","pages":"Article 102351"},"PeriodicalIF":2.5000,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Protective effect of TNIP2 on the inflammatory response of microglia after spinal cord injury in rats\",\"authors\":\"Jiawei Fu , Chunshuai Wu , Guanhua Xu , Jinlong Zhang , Jiajia Chen , Chu Chen , Hongxiang Hong , Pengfei Xue , Jiawei Jiang , Jiayi Huang , Chunyan Ji , Zhiming Cui\",\"doi\":\"10.1016/j.npep.2023.102351\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><h3>Background</h3><p>Spinal cord injury<span> (SCI) is a devastating disease that can lead to tissue loss and neurological dysfunction. TNIP2 is a negative regulator of NF-κB signaling due to its capacity to bind A20 and suppress inflammatory cytokines-induced NF-κB activation. However, the anti-inflammatory role of TNIP2 in SCI remains unclear. Our study's intention was to evaluate the effect of TNIP2 on the inflammatory response of microglia after spinal cord injury in rats.</span></p></div><div><h3>Methods</h3><p><span><span>HE </span>staining<span> and Nissl staining were performed on day 3 following SCI to analyze the histological changes. To further investigate the functional changes of TNIP2 after SCI, we performed immunofluorescence staining experiments. The effect of </span></span>LPS<span> on TNIP2 expression in BV2 cells was examined by western blot. The levels of TNF-α, IL-1β, and IL-6 in spinal cord tissues of rats with SCI and in BV2 cells with LPS were measured by using qPCR.</span></p></div><div><h3>Results</h3><p><span>TNIP2 expression was closely associated with the pathophysiology of SCI in rats, and TNIP2 was involved in regulating functional changes in microglia. TNIP2 expression was increased during SCI in rats and that overexpression of TNIP2 inhibited M1 polarization and pro-inflammatory cytokine production in microglia, which might ultimately protect against inflammatory responses through the </span>MAPK<span> and NF-κB signaling pathways.</span></p></div><div><h3>Conclusions</h3><p>The present study provides evidence for a role of TNIP2 in the regulation of inflammation in SCI and suggests that induction of TNIP2 expression alleviated the inflammatory response of microglia.</p></div>\",\"PeriodicalId\":19254,\"journal\":{\"name\":\"Neuropeptides\",\"volume\":\"101 \",\"pages\":\"Article 102351\"},\"PeriodicalIF\":2.5000,\"publicationDate\":\"2023-10-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Neuropeptides\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S014341792300032X\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"ENDOCRINOLOGY & METABOLISM\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Neuropeptides","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S014341792300032X","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"ENDOCRINOLOGY & METABOLISM","Score":null,"Total":0}
Protective effect of TNIP2 on the inflammatory response of microglia after spinal cord injury in rats
Background
Spinal cord injury (SCI) is a devastating disease that can lead to tissue loss and neurological dysfunction. TNIP2 is a negative regulator of NF-κB signaling due to its capacity to bind A20 and suppress inflammatory cytokines-induced NF-κB activation. However, the anti-inflammatory role of TNIP2 in SCI remains unclear. Our study's intention was to evaluate the effect of TNIP2 on the inflammatory response of microglia after spinal cord injury in rats.
Methods
HE staining and Nissl staining were performed on day 3 following SCI to analyze the histological changes. To further investigate the functional changes of TNIP2 after SCI, we performed immunofluorescence staining experiments. The effect of LPS on TNIP2 expression in BV2 cells was examined by western blot. The levels of TNF-α, IL-1β, and IL-6 in spinal cord tissues of rats with SCI and in BV2 cells with LPS were measured by using qPCR.
Results
TNIP2 expression was closely associated with the pathophysiology of SCI in rats, and TNIP2 was involved in regulating functional changes in microglia. TNIP2 expression was increased during SCI in rats and that overexpression of TNIP2 inhibited M1 polarization and pro-inflammatory cytokine production in microglia, which might ultimately protect against inflammatory responses through the MAPK and NF-κB signaling pathways.
Conclusions
The present study provides evidence for a role of TNIP2 in the regulation of inflammation in SCI and suggests that induction of TNIP2 expression alleviated the inflammatory response of microglia.
期刊介绍：
The aim of Neuropeptides is the rapid publication of original research and review articles, dealing with the structure, distribution, actions and functions of peptides in the central and peripheral nervous systems. The explosion of research activity in this field has led to the identification of numerous naturally occurring endogenous peptides which act as neurotransmitters, neuromodulators, or trophic factors, to mediate nervous system functions. Increasing numbers of non-peptide ligands of neuropeptide receptors have been developed, which act as agonists or antagonists in peptidergic systems.
The journal provides a unique opportunity of integrating the many disciplines involved in all neuropeptide research. The journal publishes articles on all aspects of the neuropeptide field, with particular emphasis on gene regulation of peptide expression, peptide receptor subtypes, transgenic and knockout mice with mutations in genes for neuropeptides and peptide receptors, neuroanatomy, physiology, behaviour, neurotrophic factors, preclinical drug evaluation, clinical studies, and clinical trials.
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