Anthrapyrazolone analogues intercept inflammatory JNK signals to moderate endotoxin induced septic shock.

ABSTRACT: Severe sepsis or septic shock is one of the rising causes for mortality worldwide representing nearly 10% of intensive care unit admissions. Susceptibility to sepsis is identified to be mediated by innate pattern recognition receptors and responsive signaling pathways of the host. The c-Jun N-terminal Kinase (JNK)-mediated signaling events play critical role in bacterial infection triggered multi-organ failure, cardiac dysfunction and mortality. In the context of kinase specificities, an extensive library of anthrapyrazolone analogues has been investigated for the selective inhibition of c-JNK and thereby to gain control over the inflammation associated risks. In our comprehensive biochemical characterization, it is observed that alkyl and halogen substitution on the periphery of anthrapyr

SUBMITTER: Prasad KD 

PROVIDER: S-EPMC4245532 | biostudies-literature | 2014 Nov

REPOSITORIES: biostudies-literature