自引率: 5.4%
被引量: 13709
通过率: 暂无数据
审稿周期: 3.64
版面费用: 2000
国人发稿量: 77
投稿须知/期刊简介:
Published by BioMed Central. ISSN: 1742-2094.<br /><br />Journal of Neuroinflammation is an Open Access, peer-reviewed online journal that focuses on innate immunological responses of the central nervous system, involving microglia, astrocytes, cytokines, chemokines, and related molecular processes. 'Neuroinflammation' is an encapsulization of the idea that microglial and astrocytic responses and actions in the central nervous system have a fundamentally inflammation-like character, and that these responses are central to the pathogenesis and progression of a wide variety of neurological disorders. This idea has revolutionized our understanding of Alzheimer's disease, where it originated, and now has applications to other neurodegenerative diseases, to ischemic/toxic diseases, and even to normal brain development. Neuroinflammation incorporates a wide spectrum of complex cellular responses that include microglia and astrocytes, cytokines and chemokines, complement proteins, acute phase proteins, oxidative injury, and related molecular processes. Neuroinflammation is a new and rapidly expanding field that has revolutionized our understanding of chronic neurological diseases. This field has grown to encompass researchers with backgrounds in many diverse fields, including pathology, biochemistry, molecular biology, genetics, clinical medicine, and epidemiology. Important contributions to this field have come from work with populations, with patients, with postmortem tissues, with animal models, and with in vitro systems. The Journal of Neuroinflammation will bring together work focusing on common pathogenic processes, and provide a forum for integrative reviews and commentaries on this field.
期刊描述简介:
Published by BioMed Central. ISSN: 1742-2094. Journal of Neuroinflammation is an Open Access, peer-reviewed online journal that focuses on innate immunological responses of the central nervous system, involving microglia, astrocytes, cytokines, chemokines, and related molecular processes. 'Neuroinflammation' is an encapsulization of the idea that microglial and astrocytic responses and actions in the central nervous system have a fundamentally inflammation-like character, and that these responses are central to the pathogenesis and progression of a wide variety of neurological disorders. This idea has revolutionized our understanding of Alzheimer's disease, where it originated, and now has applications to other neurodegenerative diseases, to ischemic/toxic diseases, and even to normal brain development. Neuroinflammation incorporates a wide spectrum of complex cellular responses that include microglia and astrocytes, cytokines and chemokines, complement proteins, acute phase proteins, oxidative injury, and related molecular processes. Neuroinflammation is a new and rapidly expanding field that has revolutionized our understanding of chronic neurological diseases. This field has grown to encompass researchers with backgrounds in many diverse fields, including pathology, biochemistry, molecular biology, genetics, clinical medicine, and epidemiology. Important contributions to this field have come from work with populations, with patients, with postmortem tissues, with animal models, and with in vitro systems. The Journal of Neuroinflammation will bring together work focusing on common pathogenic processes, and provide a forum for integrative reviews and commentaries on this field.
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Synergistic effects of repeated transcranial magnetic stimulation and mesenchymal stem cells transplantation on alleviating neuroinflammation and PANoptosis in cerebral ischemia.
Neuronal death is the primary cause of poor outcomes in cerebral ischemia. The inflammatory infiltration in the early phase of ischemic stroke plays a vital role in triggering neuronal death. Either transplantation of mesenchymal stem cells (MSCs) derived from humans or repetitive transcranial magnetic stimulation (rTMS) have respectively proved to be neuroprotective and anti-inflammatory in cerebral ischemia. However, either treatment above has its limitations. Whether these two therapies have synergistic effects on improving neurological function and the underlying mechanisms remains unclear. This investigation aims to elucidate the synergistic effects and underlying mechanisms of MSCs combined with rTMS treatment on the neurological function recovery post-ischemia. A Sprague-Dawley rat model of cerebral infarction was induced via transient middle cerebral artery occlusion (tMCAO). The rats were divided into five groups (n = 50): sham, tMCAO, rTMS, MSCs, and MSCs + rTMS groups. Transplantation of human umbilical cord MSCs and rTMS intervention were performed 24 h post-stroke. Neurological function was further assessed via several behavioral tests and the 2,3,5-triphenyltetrazolium chloride (TTC) staining companied with Nissl staining were used to assess neuronal survival. TUNEL staining, western blotting, immunofluorescence, immunohistochemistry, ELISA, and flow cytometry were employed to measure the levels of neuroinflammation and PANoptosis. The molecular mechanisms underlying the special role of rTMS in the combined therapy were distinguished with transcriptome sequencing via PC12 cells in oxygen-glucose deprivation/reoxygenation (OGD/R) conditions. The combined therapy efficiently reduced lesion volume and improved neuronal survival (P < 0.05), subsequently improving functional recovery after ischemic stroke. MSCs + rTMS treatment ameliorated the PANoptosis in neurons (P < 0.05), accompanied by decreased levels of inflammatory factors in the cerebral tissue and serum during the subacute phase of cerebral infarction. To further explore the roles of either therapy on synergistic effect, we found that the transplanted MSCs primarily localized in the spleen and reduced cerebral inflammatory infiltration after ischemia via suppressed splenic inflammation. Meanwhile, rTMS significantly protects neurons from PANoptosis in MSCs-inhibited inflammatory conditions by downregulating REST unveiled by transcriptome sequencing. Our study elucidates an unidentified mechanism by which the combination of MSCs and rTMS could synergistically promote neuronal survival and suppress neuroinflammation during the subacute phase of cerebral infarction, thus improving neurological outcomes. The downregulating REST induced by rTMS may potentially contribute to the neuroprotective effect against PANoptosis in MSCs-inhibited inflammatory conditions. These results are expected to provide novel insights into the mechanisms of MSCs and rTMS combination therapy in synergistically protecting against cerebral ischemia injury and potential targets underlying neuronal PANoptosis in the early phase of stroke.
被引量：- 发表：1970
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GAS6 as a potential target to alleviate neuroinflammation during Japanese encephalitis in mouse models.
被引量：- 发表：1970
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A comprehensive review of AAV-mediated strategies targeting microglia for therapeutic intervention of neurodegenerative diseases.
被引量：1 发表：1970
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iPLA2β loss leads to age-related cognitive decline and neuroinflammation by disrupting neuronal mitophagy.
被引量：- 发表：1970
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Characterization of the angiomodulatory effects of Interleukin 11 cis- and trans-signaling in the retina.
被引量：- 发表：1970
