کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6279706 | 1615080 | 2016 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Z-guggulsterone negatively controls microglia-mediated neuroinflammation via blocking IκB-α-NF-κB signals
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کلمات کلیدی
GAPDHTSTnNOSFSTeNOSiNOSIKKIκB-αIL-6LPSNF-κBDMSO - DMSOneuronal NOS - NOS عصبیinducible NOS - NOS قابل القاییForced swimming test - آزمون اجباری شناTail suspension test - آزمون تعلیق دمNeuroinflammation - التهاب عصبیendothelial NOS - اندوتلیال NOSinterleukin-6 - اینترلوکین ۶Inhibitor of κB kinase - بازدارنده kB kinasetumor necrosis factor-α - تومور نکروز عامل αCNS - دستگاه عصبی مرکزیDimethylsulfoxide - دیمتیل سولفواکسیدcentral nervous system - سیستم عصبی مرکزیTNF-α - فاکتور نکروز توموری آلفاnuclear factor κB - فاکتور هسته ای κBnuclear factor-κB - فاکتور هسته ای κBlipopolysaccharide - لیپوپلی ساکاریدNitric oxide - نیتریک اکسید
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Induction of pro-inflammatory factors is one of the characteristics of microglial activation and can be regulated by numerous active agents extracted from plants. Suppression of pro-inflammatory factors is beneficial to alleviate neuroinflammation. Z-guggulsterone, a compound extracted from the gum resin of the tree commiphora mukul, exhibits numerous anti-inflammatory effects. However, the role and mechanism of Z-guggulsterone in pro-inflammatory responses in microglia remains unclear. This study addressed this issue in in vitro murine microglia and in vivo neuroinflammation models. Results showed that Z-guggulsterone reduced inducible nitric oxide (iNOS) protein expression as well as nitric oxide (NO), tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) production in LPS-stimulated BV-2 cells. Z-guggulsterone also reduced the mRNA level of iNOS, TNF-α, and IL-6. Mechanistic studies revealed that Z-guggulsterone attenuated the LPS-induced degradation of inhibitor κ B-α (IκB-α) as well as the LPS-induced nuclear translocation of nuclear factor-κB (NF-κB). Z-guggulsterone, however, failed to reduce the LPS-induced increase in NF-κB phosphorylation level. These major findings were ascertained in primary microglia where the LPS-induced increases in iNOS expression, NO content, and IκB-α degradation were diminished by Z-guggulsterone treatment. In a mouse model of neuroinflammation, Z-guggulsterone exhibited significant anti-inflammatory effects, which were exemplified by the attenuation of microglial activation and neuroinflammation-induced behavioral abnormalities in Z-guggulsterone-treated mice. Taken together, these studies demonstrate that Z-guggulsterone attenuates the LPS-mediated induction of pro-inflammatory factors in microglia via inhibition of IκB-α-NF-κB signals, providing evidence to uncover the potential role of Z-guggulsterone in neuroinflammation-associated disorder therapies.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience Letters - Volume 619, 21 April 2016, Pages 34-42
Journal: Neuroscience Letters - Volume 619, 21 April 2016, Pages 34-42
نویسندگان
Chao Huang, Jili Wang, Xu Lu, Wenfeng Hu, Feng Wu, Bo Jiang, Yong Ling, Rongrong Yang, Wei Zhang,