高血糖通过过度激活 Toll 样受体 4 加剧氧化低密度脂蛋白诱导的许旺细胞死亡

IF 3.2 Q2 CLINICAL NEUROLOGY Neurology International Pub Date : 2024-03-19 DOI:10.3390/neurolint16020027
Wataru Nihei, Ayako Kato, Tatsuhito Himeno, Masaki Kondo, Jiro Nakamura, Hideki Kamiya, Kazunori Sango, Koichi Kato
{"title":"高血糖通过过度激活 Toll 样受体 4 加剧氧化低密度脂蛋白诱导的许旺细胞死亡","authors":"Wataru Nihei, Ayako Kato, Tatsuhito Himeno, Masaki Kondo, Jiro Nakamura, Hideki Kamiya, Kazunori Sango, Koichi Kato","doi":"10.3390/neurolint16020027","DOIUrl":null,"url":null,"abstract":"<p><p>Increased low-density lipoprotein levels are risk factors for diabetic neuropathy. Diabetes mellitus is associated with elevated metabolic stress, leading to oxidised low-density lipoprotein formation. Therefore, it is important to investigate the mechanisms underlying the pathogenesis of diabetic neuropathy in diabetes complicated by dyslipidaemia with increased levels of oxidised low-density lipoprotein. Here, we examined the effects of hyperglycaemia and oxidised low-density lipoprotein treatment on Schwann cell death and its underlying mechanisms. Immortalised mouse Schwann cells were treated with oxidised low-density lipoprotein under normo- or hyperglycaemic conditions. We observed that oxidised low-density lipoprotein-induced cell death increased under hyperglycaemic conditions compared with normoglycaemic conditions. Moreover, hyperglycaemia and oxidised low-density lipoprotein treatment synergistically upregulated the gene and protein expression of toll-like receptor 4. Pre-treatment with TAK-242, a selective toll-like receptor 4 signalling inhibitor, attenuated hyperglycaemia- and oxidised low-density lipoprotein-induced cell death and apoptotic caspase-3 pathway. Our findings suggest that the hyperactivation of toll-like receptor 4 signalling by hyperglycaemia and elevated oxidised low-density lipoprotein levels synergistically exacerbated diabetic neuropathy; thus, it can be a potential therapeutic target for diabetic neuropathy.</p>","PeriodicalId":19130,"journal":{"name":"Neurology International","volume":"16 2","pages":"370-379"},"PeriodicalIF":3.2000,"publicationDate":"2024-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10961767/pdf/","citationCount":"0","resultStr":"{\"title\":\"Hyperglycaemia Aggravates Oxidised Low-Density Lipoprotein-Induced Schwann Cell Death via Hyperactivation of Toll-like Receptor 4.\",\"authors\":\"Wataru Nihei, Ayako Kato, Tatsuhito Himeno, Masaki Kondo, Jiro Nakamura, Hideki Kamiya, Kazunori Sango, Koichi Kato\",\"doi\":\"10.3390/neurolint16020027\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Increased low-density lipoprotein levels are risk factors for diabetic neuropathy. Diabetes mellitus is associated with elevated metabolic stress, leading to oxidised low-density lipoprotein formation. Therefore, it is important to investigate the mechanisms underlying the pathogenesis of diabetic neuropathy in diabetes complicated by dyslipidaemia with increased levels of oxidised low-density lipoprotein. Here, we examined the effects of hyperglycaemia and oxidised low-density lipoprotein treatment on Schwann cell death and its underlying mechanisms. Immortalised mouse Schwann cells were treated with oxidised low-density lipoprotein under normo- or hyperglycaemic conditions. We observed that oxidised low-density lipoprotein-induced cell death increased under hyperglycaemic conditions compared with normoglycaemic conditions. Moreover, hyperglycaemia and oxidised low-density lipoprotein treatment synergistically upregulated the gene and protein expression of toll-like receptor 4. Pre-treatment with TAK-242, a selective toll-like receptor 4 signalling inhibitor, attenuated hyperglycaemia- and oxidised low-density lipoprotein-induced cell death and apoptotic caspase-3 pathway. Our findings suggest that the hyperactivation of toll-like receptor 4 signalling by hyperglycaemia and elevated oxidised low-density lipoprotein levels synergistically exacerbated diabetic neuropathy; thus, it can be a potential therapeutic target for diabetic neuropathy.</p>\",\"PeriodicalId\":19130,\"journal\":{\"name\":\"Neurology International\",\"volume\":\"16 2\",\"pages\":\"370-379\"},\"PeriodicalIF\":3.2000,\"publicationDate\":\"2024-03-19\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10961767/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Neurology International\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.3390/neurolint16020027\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"CLINICAL NEUROLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Neurology International","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.3390/neurolint16020027","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"CLINICAL NEUROLOGY","Score":null,"Total":0}
引用次数: 0

摘要

低密度脂蛋白水平升高是糖尿病神经病变的危险因素。糖尿病与代谢应激升高有关,导致氧化低密度脂蛋白的形成。因此,研究糖尿病并发血脂异常和氧化低密度脂蛋白水平升高时糖尿病神经病变的发病机制非常重要。在此,我们研究了高血糖和氧化低密度脂蛋白处理对许旺细胞死亡的影响及其内在机制。在正常或高血糖条件下,用氧化低密度脂蛋白处理永生小鼠许旺细胞。我们观察到,与正常血糖条件相比,高血糖条件下氧化低密度脂蛋白诱导的细胞死亡增加。此外,高血糖和氧化低密度脂蛋白会协同上调toll样受体4的基因和蛋白表达。使用选择性收费样受体4信号抑制剂TAK-242进行预处理可减轻高血糖和氧化低密度脂蛋白诱导的细胞死亡和细胞凋亡Caspase-3通路。我们的研究结果表明,高血糖和氧化低密度脂蛋白水平升高导致的toll样受体4信号的过度激活会协同加剧糖尿病神经病变;因此,它可以成为糖尿病神经病变的潜在治疗靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
Hyperglycaemia Aggravates Oxidised Low-Density Lipoprotein-Induced Schwann Cell Death via Hyperactivation of Toll-like Receptor 4.

Increased low-density lipoprotein levels are risk factors for diabetic neuropathy. Diabetes mellitus is associated with elevated metabolic stress, leading to oxidised low-density lipoprotein formation. Therefore, it is important to investigate the mechanisms underlying the pathogenesis of diabetic neuropathy in diabetes complicated by dyslipidaemia with increased levels of oxidised low-density lipoprotein. Here, we examined the effects of hyperglycaemia and oxidised low-density lipoprotein treatment on Schwann cell death and its underlying mechanisms. Immortalised mouse Schwann cells were treated with oxidised low-density lipoprotein under normo- or hyperglycaemic conditions. We observed that oxidised low-density lipoprotein-induced cell death increased under hyperglycaemic conditions compared with normoglycaemic conditions. Moreover, hyperglycaemia and oxidised low-density lipoprotein treatment synergistically upregulated the gene and protein expression of toll-like receptor 4. Pre-treatment with TAK-242, a selective toll-like receptor 4 signalling inhibitor, attenuated hyperglycaemia- and oxidised low-density lipoprotein-induced cell death and apoptotic caspase-3 pathway. Our findings suggest that the hyperactivation of toll-like receptor 4 signalling by hyperglycaemia and elevated oxidised low-density lipoprotein levels synergistically exacerbated diabetic neuropathy; thus, it can be a potential therapeutic target for diabetic neuropathy.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
Neurology International
Neurology International CLINICAL NEUROLOGY-
CiteScore
3.70
自引率
3.30%
发文量
69
审稿时长
11 weeks
期刊最新文献
Sensitization and Habituation of Hyper-Excitation to Constant Presentation of Pattern-Glare Stimuli. Evolution of Cognitive Disorders in Patients with Mild Cognitive Impairment (MCI) After Ischemic Stroke: Secondary Data Analysis from the Improved Health Care in Neurology and Psychiatry-Longer Life (IHCNP) Study. Macamides as Potential Therapeutic Agents in Neurological Disorders. Slow Subcutaneous Release of Glatiramer Acetate or CD40-Targeting Peptide KGYY6 Is More Advantageous in Treating Ongoing Experimental Autoimmune Encephalomyelitis. Mindfulness-Based Interventions and the Hypothalamic-Pituitary-Adrenal Axis: A Systematic Review.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1