Junjie Li, Xiaojuan Mi, Zhilun Yang, Ziqi Feng, Yong Han, Ting Wang, Haowen Lv, Yanbo Liu, Kang Wu, Juan Liu
{"title":"米诺环素通过调节小胶质细胞极化改善三叉神经痛大鼠的认知障碍","authors":"Junjie Li, Xiaojuan Mi, Zhilun Yang, Ziqi Feng, Yong Han, Ting Wang, Haowen Lv, Yanbo Liu, Kang Wu, Juan Liu","doi":"10.1016/j.intimp.2024.113786","DOIUrl":null,"url":null,"abstract":"<p><p>Trigeminal neuralgia (TN)-related cognitive impairment is a common cause of decreased quality of life in patients and is closely associated with neuroinflammation. Although minocycline has demonstrated anti-inflammatory, analgesic, and neuroprotective functions, its role in treating TN-related cognitive impairment remains unreported. In this study, we used an in vivo TN model and an in vitro model of primary microglial neuroinflammation to investigate the potential effects of minocycline on cognitive function and microglial polarization in TN rats. Our results suggested that minocycline treatment attenuated cognitive deficits by alleviating hippocampal neuronal damage and enhancing synaptic plasticity in TN rats. Furthermore, both in vitro and in vivo assays demonstrated that minocycline polarized activated microglia to the M2 phenotype, leading to the reduction of pro-inflammatory factors, including tumor necrosis factor-α and interleukin-1, and an increase in the anti-inflammatory factors, such as interleukin-4 and interleukin-10, thereby attenuating neuroinflammation. Moreover, it was found that the TLR4/MyD88/NF-κB pathway was involved in the shift of microglia from a pro-inflammatory (M1) to an anti-inflammatory (M2). In summary, minocycline likely mediated the process of microglia polarization partly via the TLR4/MyD88/NF-κB pathway, promoting neuronal survival and restoring synaptic plasticity, thereby improving TN-related cognitive impairment.</p>","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"145 ","pages":"113786"},"PeriodicalIF":4.8000,"publicationDate":"2025-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Minocycline ameliorates cognitive impairment in rats with trigeminal neuralgia by regulating microglial polarization.\",\"authors\":\"Junjie Li, Xiaojuan Mi, Zhilun Yang, Ziqi Feng, Yong Han, Ting Wang, Haowen Lv, Yanbo Liu, Kang Wu, Juan Liu\",\"doi\":\"10.1016/j.intimp.2024.113786\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Trigeminal neuralgia (TN)-related cognitive impairment is a common cause of decreased quality of life in patients and is closely associated with neuroinflammation. Although minocycline has demonstrated anti-inflammatory, analgesic, and neuroprotective functions, its role in treating TN-related cognitive impairment remains unreported. In this study, we used an in vivo TN model and an in vitro model of primary microglial neuroinflammation to investigate the potential effects of minocycline on cognitive function and microglial polarization in TN rats. Our results suggested that minocycline treatment attenuated cognitive deficits by alleviating hippocampal neuronal damage and enhancing synaptic plasticity in TN rats. Furthermore, both in vitro and in vivo assays demonstrated that minocycline polarized activated microglia to the M2 phenotype, leading to the reduction of pro-inflammatory factors, including tumor necrosis factor-α and interleukin-1, and an increase in the anti-inflammatory factors, such as interleukin-4 and interleukin-10, thereby attenuating neuroinflammation. Moreover, it was found that the TLR4/MyD88/NF-κB pathway was involved in the shift of microglia from a pro-inflammatory (M1) to an anti-inflammatory (M2). In summary, minocycline likely mediated the process of microglia polarization partly via the TLR4/MyD88/NF-κB pathway, promoting neuronal survival and restoring synaptic plasticity, thereby improving TN-related cognitive impairment.</p>\",\"PeriodicalId\":13859,\"journal\":{\"name\":\"International immunopharmacology\",\"volume\":\"145 \",\"pages\":\"113786\"},\"PeriodicalIF\":4.8000,\"publicationDate\":\"2025-01-03\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"International immunopharmacology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1016/j.intimp.2024.113786\",\"RegionNum\":2,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2024/12/12 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q2\",\"JCRName\":\"IMMUNOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"International immunopharmacology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1016/j.intimp.2024.113786","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/12/12 0:00:00","PubModel":"Epub","JCR":"Q2","JCRName":"IMMUNOLOGY","Score":null,"Total":0}
Minocycline ameliorates cognitive impairment in rats with trigeminal neuralgia by regulating microglial polarization.
Trigeminal neuralgia (TN)-related cognitive impairment is a common cause of decreased quality of life in patients and is closely associated with neuroinflammation. Although minocycline has demonstrated anti-inflammatory, analgesic, and neuroprotective functions, its role in treating TN-related cognitive impairment remains unreported. In this study, we used an in vivo TN model and an in vitro model of primary microglial neuroinflammation to investigate the potential effects of minocycline on cognitive function and microglial polarization in TN rats. Our results suggested that minocycline treatment attenuated cognitive deficits by alleviating hippocampal neuronal damage and enhancing synaptic plasticity in TN rats. Furthermore, both in vitro and in vivo assays demonstrated that minocycline polarized activated microglia to the M2 phenotype, leading to the reduction of pro-inflammatory factors, including tumor necrosis factor-α and interleukin-1, and an increase in the anti-inflammatory factors, such as interleukin-4 and interleukin-10, thereby attenuating neuroinflammation. Moreover, it was found that the TLR4/MyD88/NF-κB pathway was involved in the shift of microglia from a pro-inflammatory (M1) to an anti-inflammatory (M2). In summary, minocycline likely mediated the process of microglia polarization partly via the TLR4/MyD88/NF-κB pathway, promoting neuronal survival and restoring synaptic plasticity, thereby improving TN-related cognitive impairment.
期刊介绍:
International Immunopharmacology is the primary vehicle for the publication of original research papers pertinent to the overlapping areas of immunology, pharmacology, cytokine biology, immunotherapy, immunopathology and immunotoxicology. Review articles that encompass these subjects are also welcome.
The subject material appropriate for submission includes:
• Clinical studies employing immunotherapy of any type including the use of: bacterial and chemical agents; thymic hormones, interferon, lymphokines, etc., in transplantation and diseases such as cancer, immunodeficiency, chronic infection and allergic, inflammatory or autoimmune disorders.
• Studies on the mechanisms of action of these agents for specific parameters of immune competence as well as the overall clinical state.
• Pre-clinical animal studies and in vitro studies on mechanisms of action with immunopotentiators, immunomodulators, immunoadjuvants and other pharmacological agents active on cells participating in immune or allergic responses.
• Pharmacological compounds, microbial products and toxicological agents that affect the lymphoid system, and their mechanisms of action.
• Agents that activate genes or modify transcription and translation within the immune response.
• Substances activated, generated, or released through immunologic or related pathways that are pharmacologically active.
• Production, function and regulation of cytokines and their receptors.
• Classical pharmacological studies on the effects of chemokines and bioactive factors released during immunological reactions.