|1.||Bennett, Brydon L: 6 articles (07/2007 - 12/2003)|
|2.||Shyu, Kou-Gi: 4 articles (01/2015 - 02/2008)|
|3.||Wang, Bao-Wei: 4 articles (01/2015 - 02/2008)|
|4.||Zhang, Guang-Yi: 4 articles (11/2011 - 02/2005)|
|5.||Adcock, Ian M: 4 articles (07/2007 - 12/2003)|
|6.||Nath, Puneeta: 4 articles (07/2007 - 12/2003)|
|7.||Guan, Qiu-Hua: 4 articles (05/2007 - 02/2005)|
|8.||Pei, Dong-Sheng: 4 articles (05/2007 - 02/2005)|
|9.||Chen, Yen-Chou: 3 articles (01/2014 - 12/2010)|
|10.||Shen, Shing-Chuan: 3 articles (01/2014 - 12/2010)|
05/01/2006 - "The specific JNK inhibitor SP600125 targets tumour necrosis factor-alpha production and epithelial cell apoptosis in acute murine colitis."
10/01/2014 - "In mice with type 1 diabetes, the administration of C66 or SP600125 at 5 mg/kg significantly decreased the levels of plasma and cardiac tumor necrosis factor-α, accompanied by decreasing cardiac apoptosis, and, finally, improved histological abnormalities, fibrosis, and cardiac dysfunction without affecting hyperglycemia. "
07/01/2010 - "Nuclear DNA fragmentation, nitrotyrosine staining, tissue GSSG levels and liver injury (plasma ALT release and necrosis) were partially attenuated by the vehicle (-65%) and completely eliminated by SP600125 (-98%) at 6 and 12h. "
10/01/2015 - "The effects on the phosphorylation of MAP kinases (c-Jun N-terminal kinases (JNKs), p38) and activation of nuclear factor-kappa B (NF-κB) pathways of 1 and its 1H-indazole-containing analogue 3, compared with those elicited by the known Adenosine Triphosphate (ATP)-competitive JNK inhibitor SP600125, were evaluated through Western blot analysis in murine fibroblasts NIH-3T3 and human endothelial cells EA.hy926 acutely treated with tumour necrosis factor-α (TNF-α). "
07/01/2010 - "Our data suggest that the JNK inhibitor SP600125 protects against APAP-induced liver injury in part by attenuation of mitochondrial Bax translocation but mainly by preventing mitochondrial oxidant stress and peroxynitrite formation and thereby preventing the mitochondrial permeability transition pore opening, a key event in APAP-induced cell necrosis."
05/01/2012 - "[Protective effects and mechanism of SP600125 on lung ischemia/reperfusion injury in rats]."
07/01/2011 - "Protective effects of SP600125 on renal ischemia-reperfusion injury in rats."
08/31/2006 - "SP600125, a selective JNK inhibitor, aggravates hepatic ischemia-reperfusion injury."
05/01/2012 - "SP600125 can suppress JNK signal pathway, up-regulate the ratio of Bcl-2/Bax to inhibit Caspase-3 dependent apoptosis, so that it protects lung tissue from ischemia/reperfusion injury."
11/01/2009 - "Sixty rats were randomly divided into six groups: sham, reperfusion injury (R/I), postconditioning (Post), SP600125 (I_JNK), anisomycin and postconditioning (Ani+Post) and anisomycin (Ani) groups. "
01/01/2015 - "Interestingly, treatment with SP600125 significantly decreased the incidence of lesions and also protected against vascular inflammation and tissue destruction histologically, compared with the placebo treatment. "
05/01/2013 - "The promising findings of this study make SP600125 a potential agent for supportive therapy to alleviate inflammation and neuronal cell death associated with CM."
01/01/2009 - "SP600125 has the potential to remarkably attenuate steatosis and inflammation and may be a novel therapeutic drug against NASH."
11/01/2013 - "MAPKs' inhibitors could reduce mechanical ventilation-induced inflammation, and SP600125 produced the most robust decrease in inflammation. "
10/01/2015 - "In the present study, we aimed to investigate the effect of the JNK inhibitor SP600125 on the resolution of airway inflammation, and the underlying mechanism using a murine acute asthma model. "
|4.||Brain Injuries (Brain Injury)
05/30/2006 - "Neuroprotection against ischemic brain injury by SP600125 via suppressing the extrinsic and intrinsic pathways of apoptosis."
02/21/2005 - "To further study the roles of JNK activation in hippocampal CA1 neurons in a rat model of transient global ischemia, we assessed the effect of JNK inhibition by SP600125 on the degree of brain injury. "
02/01/2012 - "The present results indicate that SP600125 can dramatically improve trauma brain injury from autophagy after DBI and the molecular mechanism is related to the modulation of JNK signal pathway following DBI, while it measures the neuron autophagy by means of intervening JNK signal pathway."
08/01/2012 - "The aim of this study is to investigate whether the protective effects of SP600125 were associated with modulation of tight junction proteins including claudin-5 and ZO-1 and to define which JNK isoforms were involved in the early brain injury after SAH. "
04/01/2005 - "We hypothesize that inhibiting JNK will lead to the inhibition of tumor growth; therefore, we evaluated the efficacy of the recently described JNK inhibitor SP600125 [anthra[1,9-cd] pyrazol-6 (2H)-one]. "
05/01/2014 - "Treatment of parental cells with SP600125, a c-JUN-NH2-kinase (JNK) inhibitor, recapitulated defects in EPHA2-deficient tumor cells, whereas constitutively activated JNK mutants were sufficient to rescue phenotypes. "
01/01/2014 - "UA in combination with the pan-JNK inhibitor SP600125 showed maximal reduction in viability across a panel of cancer cell lines, thereby corroborating our predictive simulation assays. "
10/01/2013 - "Furthermore, A549 cells either pre-treated with SP600125 or transiently transfected with siRNAs against the JNK genes in vitro showed substantially reduced ability to initiate tumor formation upon implantation into nude mice, implying that the cell intrinsic JNK activity of A549 cells is essential for the maintenance of their tumor-initiating capacity. "
10/01/2013 - "Nevertheless, the same SP600125 treatment caused a marked reduction in the tumor-initiating population within the A549 tumors, suggesting that JNK may be specifically required in vivo for the maintenance of the tumor-initiating population of tumor cells rather than for proliferation and survival of the entire cell population. "
|1.||JNK Mitogen-Activated Protein Kinases
|2.||Proteins (Proteins, Gene)
|4.||Protein Isoforms (Isoforms)
|5.||Mitogen-Activated Protein Kinase 3
|8.||Nerve Growth Factor (NGF)
|9.||Glutathione Disulfide (GSSG)
|10.||Amyloid (Amyloid Fibrils)
|1.||Heterologous Transplantation (Xenotransplantation)
|4.||Artificial Respiration (Mechanical Ventilation)
|5.||Nebulizers and Vaporizers (Inhaler)