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10.2119/molmed.2014.00199 http://scihub22266oqcxt.onion/10.2119/molmed.2014.00199 C4503649!4503649 !25811992     free     free     free Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\25811992 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Mol+Med 2015 ; 21 (1 ): 197-209 Nephropedia Template TP {{tp|p=25811992 |t=2015. Acetylbritannilactone Modulates MicroRNA-155-Mediated Inflammatory Response in Ischemic Cerebral Tissues |pdf=|usr=}}{{25811992 }} gab.com Text Acetylbritannilactone Modulates MicroRNA-155-Mediated Inflammatory Response in Ischemic Cerebral Tissues JO: Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=25811992 #FOAvip Inflammatory responses play a critical role in ischemic brain injury. MicroRNA-155 (miR-155) induces the expression of inflammatory cytokines, and acetylbritannilactone (ABL) exerts potent antiinflammatory actions by inhibiting expression of inflammation-related genes. However, the functions of miR-155 and the actual relationship between ABL and miR-155 in ischemia-induced cerebral inflammation remain unclear. In this study, cerebral ischemia of wild-type (WT) and miR-155(-/-) mice was induced by permanent middle cerebral artery occlusion (MCAO). pAd-miR-155 was injected into the lateral cerebral ventricle 24 h before MCAO to induce miR-155 overexpression. MCAO mice and oxygen-glucose deprivation (OGD)-treated BV2 cells were used to examine the effects of ABL and miR-155 overexpression or deletion on the expression of proinflammatory cytokines. We demonstrated that ABL treatment significantly reduced neurological deficits and cerebral infarct volume by inhibiting tumor necrosis factor-? (TNF-?) and interleukin-1? (IL-1?) expression in ischemic cerebral tissue and OGD-treated BV2 cells. Mechanistic studies suggested that the observed decrease in TNF-? and IL-1? expression was attributable to the ABL-induced suppression of the expression of nuclear factor-kappa B (NF-?B) and Toll-like receptor 4 (TLR4). We further found that miR-155 promoted TNF-? and IL-1? expression by upregulating TLR4 and downregulating the expression of suppressor of cytokine signaling 1 (SOCS1) and myeloid differentiation primary response gene 88 (MyD88), while ABL exerted an inhibitory effect on miR-155-mediated gene expression. In conclusion, miR-155 mediates inflammatory responses in ischemic cerebral tissue by modulating TLR4/MyD88 and SOCS1 expression, and ABL exerts its antiinflammatory action by suppressing miR-155 expression, suggesting a novel miR-155-based therapy for ischemic stroke. Twit Text FOAVip Acetylbritannilactone Modulates MicroRNA-155-Mediated Inflammatory Response in Ischemic Cerebral Tissues ????Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=25811992 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25811992 #FOAvip English Wikipedia <ref>{{Cite pmid|25811992 }}</ref> Acetylbritannilactone Modulates MicroRNA-155-Mediated Inflammatory Response in Ischemic Cerebral Tissues #MMPMID25811992 Wen Y ; Zhang X ; Dong L ; Zhao J ; Zhang C ; Zhu C Mol Med 2015[Mar]; 21 (1 ): 197-209 PMID25811992 show ga Inflammatory responses play a critical role in ischemic brain injury. MicroRNA-155 (miR-155) induces the expression of inflammatory cytokines, and acetylbritannilactone (ABL) exerts potent antiinflammatory actions by inhibiting expression of inflammation-related genes. However, the functions of miR-155 and the actual relationship between ABL and miR-155 in ischemia-induced cerebral inflammation remain unclear. In this study, cerebral ischemia of wild-type (WT) and miR-155(-/-) mice was induced by permanent middle cerebral artery occlusion (MCAO). pAd-miR-155 was injected into the lateral cerebral ventricle 24 h before MCAO to induce miR-155 overexpression. MCAO mice and oxygen-glucose deprivation (OGD)-treated BV2 cells were used to examine the effects of ABL and miR-155 overexpression or deletion on the expression of proinflammatory cytokines. We demonstrated that ABL treatment significantly reduced neurological deficits and cerebral infarct volume by inhibiting tumor necrosis factor-? (TNF-?) and interleukin-1? (IL-1?) expression in ischemic cerebral tissue and OGD-treated BV2 cells. Mechanistic studies suggested that the observed decrease in TNF-? and IL-1? expression was attributable to the ABL-induced suppression of the expression of nuclear factor-kappa B (NF-?B) and Toll-like receptor 4 (TLR4). We further found that miR-155 promoted TNF-? and IL-1? expression by upregulating TLR4 and downregulating the expression of suppressor of cytokine signaling 1 (SOCS1) and myeloid differentiation primary response gene 88 (MyD88), while ABL exerted an inhibitory effect on miR-155-mediated gene expression. In conclusion, miR-155 mediates inflammatory responses in ischemic cerebral tissue by modulating TLR4/MyD88 and SOCS1 expression, and ABL exerts its antiinflammatory action by suppressing miR-155 expression, suggesting a novel miR-155-based therapy for ischemic stroke. |Animals [MESH] |Brain Ischemia/*genetics/*metabolism/pathology [MESH] |Cell Line [MESH] |Disease Models, Animal [MESH] |Gene Expression [MESH] |Gene Expression Regulation/drug effects [MESH] |Inflammation/*genetics/*metabolism/pathology [MESH] |Lactones/*metabolism/pharmacology [MESH] |Male [MESH] |Mice [MESH] |Mice, Knockout [MESH] |MicroRNAs/*genetics [MESH] |Microglia/metabolism [MESH] |Myeloid Differentiation Factor 88/genetics/metabolism [MESH] |NF-kappa B/metabolism [MESH] |Signal Transduction [MESH] |Suppressor of Cytokine Signaling 1 Protein [MESH] |Suppressor of Cytokine Signaling Proteins/genetics/metabolism [MESH]Acetylbritannilactone Modulates MicroRNA-155-Mediated Inflammatory Res(epmc).pdf DeepDyve Pubget Overpricing