http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Autophagy in the liver: cell’s cannibalism and beyond
Joseph A. Flores-Toro,Kristina L. Go,Christiaan Leeuwenburgh,Jae-Sung Kim 대한약학회 2016 Archives of Pharmacal Research Vol.39 No.8
Chronic liver disease and its progression to liverfailure are induced by various etiologies including viralinfection, alcoholic and nonalcoholic hepatosteatosis. It isanticipated that the prevalence of fatty liver disease willcontinue to rise due to the growing incidence of obesity andmetabolic disorder. Evidence is accumulating to indicatethat the onset of fatty liver disease is causatively linked tomitochondrial dysfunction and abnormal lipid accumulation. Current treatment options for this disease are limited. Autophagy is an integral catabolic pathway that maintainscellular homeostasis both selectively and nonselectively. As mitophagy and lipophagy selectively remove dysfunctionalmitochondria and excess lipids, respectively, stimulationof autophagy could have therapeutic potential toameliorate liver function in steatotic patients. This reviewhighlights our up-to-date knowledge on mechanistic rolesof autophagy in the pathogenesis of fatty liver disease andits vulnerability to surgical stress, with an emphasis onmitophagy and lipophagy.
Inhibition of NF-κB-induced inflammatory responses by angiotensin II antagonists in aged rat kidney
Kim, J.M.,Heo, H.S.,Choi, Y.J.,Ye, B.H.,Mi Ha, Y.,Seo, A.Y.,Yu, B.P.,Leeuwenburgh, C.,Chung, H.Y.,Carter, C.S. Pergamon Press ; Elsevier Science Ltd 2011 Experimental Gerontology Vol.46 No.7
In this study, we explored the mechanisms by which the angiotensin converting enzyme inhibitor (ACEI), enalapril, and the Ang II receptor blocker (ARB), losartan suppress oxidative stress and NF-κB activation-induced inflammatory responses in aged rat kidney. The experimentations were carried out utilizing aged (24-month-old) Brown NorwayxFischer 344 (F1) male rats which were randomized into 3 groups and administered enalapril (40mg/kg), losartan (30mg/kg) or placebo for 6months (daily p.o.). The level of reactive species (RS), peroxynitrite (ONOO<SUP>-</SUP>), GSH/GSSG and lipid peroxidation were measured. The activity of the pro-inflammatory transcription factor NF-κB, and gene expression of proteins in upstream signaling cascades were measured by electro-mobility shift assay (EMSA) and Western blotting. Enalapril and losartan differentially attenuated redox imbalance and the redox-sensitive transcription factor, the NF-κB pathway. Furthermore, stimulation of the NF-κB activation pathway by phosphorylation of p65 was attenuated by both compounds. Moreover, mediation of phosphorylation of p65 by phosphorylation of IκB kinase αβ (IKKαβ) and mitogen- and stress-activated protein kinase-1 (MSK-1), were also inhibited by enalapril and losartan. Finally, both compounds also lowered expression of NF-κB-dependent inflammatory genes, such as cyclooxygenase-2 (COX-2), and inducible NO synthase (iNOS). Only losartan lowered levels of 5-lipoxygenase (5-LOX). These findings indicate that enalapril and losartan differentially suppress inflammatory responses via inhibition of oxidative stress-induced NF-κB activation in aged rat kidney.