NF-κB inhibitors stabilize the mRNA of high-affinity type-2 cationic amino acid transporter in LPS-stimulated rat liver

摘要: Background:  Induction of inducible nitric oxide synthase (iNOS) results in (NO) overproduction during endotoxemia. Cellular uptake l-arginine, modulated by the isozymes type-2 cationic amino acid transporters (CAT), including CAT-2, CAT-2A and CAT-2B, has been reported to be a crucial factor regulation iNOS activity. We sought elucidate expression CAT-2 role nuclear factor-κB (NF-κB) this lipopolysaccharide (LPS)-treated rat liver. Methods:  Adult male Sprague–Dawley rats were randomly given intravenous (i.v.) injections normal saline (N/S), LPS, LPS preceded an NF-κB inhibitor (PDTC, dexamethasone or salicylate) alone. After injection, sacrificed at different times enzyme liver injury examined. Hepatic systemic NO production also measured. Results:  CAT-2B constitutively expressed un-stimulated liver. stimulation not only significantly increased mRNA concentrations but decreased CAT-2A, time-dependent manner. LPS-induced hepatic was associated with hepatocellular injury. Pre-treatment inhibitors attenuated induction as well CAT-2/CAT-2B destabilization, which significant inhibition biosynthesis less injury. Conclusion:  stabilize LPS-stimulated The pathway may constitutive part cytoprotective mechanisms against sepsis.