Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P05412 (c-Jun)
 11,453 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The c-Jun NH(2)-terminal kinase (JNK), also known as stress-activated protein kinase, is a mitogen-activated protein kinase that determines cell survival in response to environmental stress. Activation of JNK involves redox-sensitive mechanisms and physiological stimuli such as shear stress, the dragging force generated by blood flow over the endothelium. Laminar shear stress has antiatherogenic properties and controls structure and function of endothelial cells by mechanisms including production of nitric oxide (NO) and superoxide (O(-)(2)). Here we show that both NO and O(-)(2) are required for activation of JNK by shear stress in endothelial cells. The present study also demonstrates that exposure of endothelial cells to shear stress increases tyrosine nitration, a marker of reactive nitrogen species formation. Furthermore, inhibitors or scavengers of NO, O(-)(2), or reactive nitrogen species prevented shear-dependent increase in tyrosine nitration and activation of JNK. Peroxynitrite alone, added to cells as a bolus or generated over 60 min by 3-morpholinosydnonimine, also activates JNK. These results suggest that reactive nitrogen species, in this case most likely peroxynitrite, act as signaling molecules in the mechanoactivation of JNK.
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PMID:Evidence for peroxynitrite as a signaling molecule in flow-dependent activation of c-Jun NH(2)-terminal kinase. 1051 6

Scutellarin is a natural compound from a Chinese herb. The purpose of this paper was to study the protective effect of scutellarin on concanavalin A (Con A)-induced immunological liver injury and its effect on liver nuclear factor kappaB (NF-kappaB), tumor necrosis factor alpha (TNF-alpha), interferon gamma (IFN-gamma), and inducible nitric oxide synthase (iNOS) expression in mice. Mouse liver injury was produced by injection of Con A 25 mg kg-1 via the tail vein. Scutellarin 50 or 100 mg kg-1 was peritoneally administered to mice 9 or 1 h before injection of Con A. The levels of serum alanine aminotransferase (ALT) and asparatate aminotransferase (AST), NO2-/NO3- and TNF-alpha were determined with biochemical kits, and ELISA using Quantikine Mouse TNF-alpha kit according the manufacturer's instructions. Liver lesions were examined by light microscope. The expression of TNF-alpha, IFN-gamma, iNOS and Fas mRNA in the livers was detected by RT-PCR; and the expression of c-Fos, c-Jun, iNOS and IkappaB proteins was measured by Western Blotting. As a result, pretreatment with scutellarin 100 mg kg-1 significantly decreased the serum ALT, AST, NO2-/NO3- and TNF-alpha levels, and also reduced liver lesions induced by Con A. Scutellarin 100 mg kg-1 down-regulated expression of TNF-alpha and iNOS mRNA, and c-Fos, c-Jun and iNOS protein, while scutellarin enhanced the degradation of IkappaB in the livers of mice injected with Con A. The results suggest that scutellarin has a protective action against Con A-induced liver injury in mice, and its active mechanism may be related to the inhibition of the NF-kappaB-TNF-alpha-iNOS transduction pathway.
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PMID:The protective action of scutellarin against immunological liver injury induced by concanavalin A and its effect on pro-inflammatory cytokines in mice. 1722 28

This paper investigates the effect of natural scutellarin on acute lung injury (ALI) induced by Escherichia coli endotoxin lipopolysaccharide (LPS) in mice and its mechanism of action. Mouse ALI was induced by the injection of LPS (15 mg/kg) via the tail vein, and mice were intraperitoneally injected with 50 and 25 mg/kg of scutellarin before the LPS injection. The lung index, serum NO2(-)/NO3(-), and tumor necrosis factor-alpha (TNF-alpha) levels were determined using kits. The lung lesions were examined by light microscope. The mRNA levels of TNF-alpha, inducible nitric oxide synthase (iNOS), and FasL in pulmonary tissues were detected by RT-PCR. c-Fos, c-Jun, IkappaB, and iNOS proteins were detected by the western blotting method. Pretreatment with 25 and 50 mg/kg of scutellarin significantly reduced lung injury induced by LPS, which expressed in the decrease in lung morphological lesions, serum NO2(-)/NO3(-), TNF-alpha levels, lactate dehydrogenase release, and total protein in the lavage fluid of bronchoalveolar of the lung. The mRNA level of TNF-alpha, iNOS, the protein content of c-Fos, iNOS, and the activation of NF-kappaB in pulmonary tissues were all inhibited, while the lung glutathione level increased. In conclusion, scutellarin has protective action against LPS-induced lung damage in mice, and its underlying mechanism might be the inhibition of IkappaB alpha degradation and the expression of TNF-alpha mRNA.
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PMID:Scutellarin protects against lipopolysaccharide-induced acute lung injury via inhibition of NF-kappaB activation in mice. 2039 Jul 62