کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
11019371 | 1718112 | 2018 | 12 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Isoliquiritigenin protects against bloodâbrain barrier damage and inhibits the secretion of pro-inflammatory cytokines in mice after traumatic brain injury
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
ایمنی شناسی و میکروب شناسی
ایمونولوژی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Traumatic brain injury (TBI) caused by an external mechanical force acting on the brain is a serious neurological condition. Inflammation plays an important role in prolonging secondary tissue injury after TBI, leading to neuronal cell death and dysfunction. Isoliquiritigenin (ILG) is a flavonoid monomer with anti-inflammatory characteristic. Thus, we had investigated the potential protective effects of ILG on TBI-induced injuries and identified the mechanisms underlying it. Here, we have demonstrated that ILG preserves blood brain barrier (BBB) integrity in vivo, suppresses the activation of microglia and inflammatory responses in mice after TBI, consequently leading to neurofunctional deficits, brain oedema, structural damage, and macrophage infiltration. In vitro, ILG exerts anti-inflammatory effect, and upregulates tight junction proteins 120âβâcatenin and occludin in SHâSY5Y cells under oxygen glucose deprivation/reoxygenation (OGD/D) condition. Additionally, we found that PI3K/AKT/GSKâ3β signalling pathway is involved in ILG treatment for TBI. To further confirm it, we had used SC79 (ethyl 2âaminoâ6âchloroâ4â(1âcyanoâ2âethoxyâ2âoxoethyl)â4Hâchromeneâ3âcarboxylate), an Akt specific activator, to activate Akt, we found that SC79 partially reduces the protective effect of ILG for TBI. Overall, our current study reveals the neuroprotective role of ILG on TBI-induced BBB damage, downregulated tight junction proteins via PI3K/AKT/GSKâ3β signalling pathway. Furthermore, ILG suppresses the secretion of pro-inflammatory cytokines after TBI through inhibiting the PI3K/AKT/GSKâ3β/NFâκB signalling pathway. Our findings suggest that GSKâ3β is a key regulatory factor during TBI-induced secretion of inflammatory cytokines, neuronal apoptosis and destruction of BBB.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: International Immunopharmacology - Volume 65, December 2018, Pages 64-75
Journal: International Immunopharmacology - Volume 65, December 2018, Pages 64-75
نویسندگان
Man Zhang, Yanqing Wu, Ling Xie, Chen-Huai Teng, Fang-Fang Wu, Ke-Bin Xu, Xiong Chen, Jian Xiao, Hong-Yu Zhang, Da-Qing Chen,