• Filter By:
• Specialty
• Source
• Condition
• Cancer
• Infectious Disease
• Drug
• Training
• Management
• Procedure
• Therapy
• Vaccine
• Nutrition
• Country

S1PR3 is essential for phosphorylated fingolimod to protect astrocytes against oxygen-glucose deprivation-induced neuroinflammation via inhibiting TLR2/4-NF κB signalling.
This study was intended to investigate the mechanisms of phosphorylated FTY720 (pFTY720), which was the principle active molecule in regulating astrocyte-mediated inflammatory responses induced by oxygen-glucose deprivation (OGD). Results demonstrated that pFTY720 could protect astrocytes against OGD-induced injury and inflammatory responses. It significantly decreased pro-inflammatory cytokines, including high mobility group box 1 (HMGB1) and tumour necrosis factor-α (TNF-α). Further, studies displayed that pFTY720 could prevent up-regulation of Toll-like receptor 2 (TLR2), phosphorylation of phosphoinositide 3-kinase (...
Source: J Cell Mol Med - March 13, 2018 Category: Molecular Biology Authors: Dong YF, Guo RB, Ji J, Cao LL, Zhang L, Chen ZZ, Huang JY, Wu J, Lu J, Sun XL Tags: J Cell Mol Med Source Type: research

S1PR3 is essential for phosphorylated fingolimod to protect astrocytes against oxygen ‐glucose deprivation‐induced neuroinflammation via inhibiting TLR2/4‐NFκB signalling
This study was intended to investigate the mechanisms of phosphorylated FTY720 (pFTY720), which was the principle active molecule in regulating astrocyte‐mediated inflammatory responses induced by oxygen‐glucose deprivation (OGD). Results demonstrated that pFTY720 could protect astrocytes against OGD‐induced injury and inflammatory responses. It significantly decreased pro‐inflammatory cytokines, including high mobility group box 1 (HMGB1) and tumour necrosis factor‐α (TNF‐α). Further, studies displayed that pFTY720 could prevent up‐regulation of Toll‐like receptor 2 (TLR2), phosphorylation of phosphoinos...
Source: Journal of Cellular and Molecular Medicine - March 13, 2018 Category: Molecular Biology Authors: Yin ‐Feng Dong, Ruo‐Bing Guo, Juan Ji, Lu‐Lu Cao, Ling Zhang, Zheng‐Zhen Chen, Ji‐Ye Huang, Jin Wu, Jun Lu, Xiu‐Lan Sun Tags: ORIGINAL ARTICLE Source Type: research