pyrazolanthrone

01/01/2019 - "The results show that acute inflammation is an adaptive and controlled response to the SP600125-stress, which is beneficial for alleviating toxicity by SP600125. "
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. "
10/15/2021 - "Our results indicated that SP600125 rescued the chondrogenesis of BMSCs by inhibiting inflammation induced by TNF-α, which provides a theoretical basis for solving the problem of cartilage repair under inflammatory conditions."
09/01/2021 - "The addition of an AP‑1 inhibitor (SP600125) further inhibited pathway activity, and IL‑13‑induced inflammation and mucus formation was restored. "
12/01/2020 - "Inhibition of inflammation by SP600125 in cholestatic liver injury is dependent on the administration‑based exposure profile."

01/01/2016 - "We identified JNK signaling as a potential area of intervention and now show that inhibiting JNK using the pan-JNK inhibitor, SP600125, is effective in the HER2-positive, resistant JIMT-1 xenograft mammary tumor model. "
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]. "
01/01/2019 - "Murine xenograft models were established to determine the effect of DEPDC1 on tumor growth in vivo SP600125, a JNK specific inhibitor, was applied to carriy out mechanistic studies. "
08/01/2021 - "SP600125 significantly decreased tumor volume and induced spindle-shaped tumor cells in vivo. "
08/01/2021 - "The effects of Dkk-1 and SP600125 on cell proliferation, in vivo tumor growth, and bone tumor phenotype were investigated. "

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."
02/05/2021 - "Treatment with SP600125, an inhibitor of c-Jun N-terminal kinase (JNK), can suppress the JNK signaling pathway to alleviate donor liver ischemia-reperfusion injury (IRI). "
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."

03/01/2006 - "In a neonatal mouse model of GBS sepsis SP600125 inhibited the inflammatory response and improved survival. "
01/01/2015 - "SP600125 protects against CLP induced sepsis by blocking JNK signalling; therefore, it can be considered a therapeutic approach in human sepsis. "
01/01/2019 - "Protective role of JNK inhibitor SP600125 in sepsis-induced acute lung injury."
01/01/2020 - "Accordingly, genetic ablation of BNP, as well as treatment with a potentially novel neutralizing anti-BNP monoclonal antibody (19B3) or suppression of its expression via administration of JNK inhibitor SP600125 improved cardiac output, stabilized blood pressure, and improved survival in mice with polymicrobial sepsis. "
01/01/2015 - "Aim of our study was to evaluate the effects of SP600125, a specific c-Jun NH2-terminal kinase (JNK) inhibitor, to modulate the early and late steps of the inflammatory cascade in a murine model of CLP-induced sepsis. "

05/01/2006 - "The specific JNK inhibitor SP600125 targets tumour necrosis factor-alpha production and epithelial cell apoptosis in acute murine colitis."
01/01/2020 - "The addition of either autophagy inhibitors (3-methyladenine or wortmannin) or SP600125 corrected the combined regimen-triggered S-phase arrest, whereas had little effect on the apoptosis/necrosis induction in the cells. "
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. "
05/01/2016 - "Additionally, the inhibition of JNK with SP600125 repressed the apoptotic cell death induced by RCM extract, ellagic acid and quercetin, and the inhibition of JNK appeared to switch apoptosis to necrosis. "
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. "