Recombinant Human Thioredoxin-1 Protects Macrophages from Oxidized Low-Density Lipoprotein-Induced Foam Cell Formation and Cell Apoptosis

Zhang, Hui; Liu, Qi; Lin, Jia-Le; Wang, Yu; Zhang, Ruo-Xi; Hou, Jing-Bo; Yu, Bo

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자료유형: 학술저널

저자정보: Zhang, Hui (Department of Cardiology, Key Laboratories of Education Ministry for Myocardial Ischemia Mechanism and Treatment, the Second Affiliated Hospital of Harbin Medical University) Liu, Qi (Department of Cardiology, Key Laboratories of Education Ministry for Myocardial Ischemia Mechanism and Treatment, the Second Affiliated Hospital of Harbin Medical University) Lin, Jia-Le (Department of Cardiology, Key Laboratories of Education Ministry for Myocardial Ischemia Mechanism and Treatment, the Second Affiliated Hospital of Harbin Medical University) Wang, Yu (Department of Cardiology, Key Laboratories of Education Ministry for Myocardial Ischemia Mechanism and Treatment, the Second Affiliated Hospital of Harbin Medical University) Zhang, Ruo-Xi (Department of Cardiology, Key Laboratories of Education Ministry for Myocardial Ischemia Mechanism and Treatment, the Second Affiliated Hospital of Harbin Medical University) Hou, Jing-Bo (Department of Cardiology, Key Laboratories of Education Ministry for Myocardial Ischemia Mechanism and Treatment, the Se) Yu, Bo

저널정보: 한국응용약물학회 Biomolecules & Therapeutics(구 응용약물학회지) Biomolecules & therapeutics 제26권 제2호

발행연도: 2018.1

수록면: 121 - 129 (9page)

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Oxidized low-density lipoprotein (ox-LDL)-induced macrophage foam cell formation and apoptosis play critical roles in the pathogenesis of atherosclerosis. Thioredoxin-1 (Trx) is an antioxidant that potently protects various cells from oxidative stress-induced cell death. However, the protective effect of Trx on ox-LDL-induced macrophage foam cell formation and apoptosis has not been studied. This study aims to investigate the effect of recombinant human Trx (rhTrx) on ox-LDL-stimulated RAW264.7 macrophages and elucidate the possible mechanisms. RhTrx significantly inhibited ox-LDL-induced cholesterol accumulation and apoptosis in RAW264.7 macrophages. RhTrx also suppressed the ox-LDL-induced overproduction of lectin-like oxidized LDL receptor (LOX-1), Bax and activated caspase-3, but it increased the expression of Bcl-2. In addition, rhTrx markedly inhibited the ox-LDL-induced production of intracellular reactive oxygen species (ROS) and phosphorylation of p38 mitogen-activated protein kinases (MAPK). Furthermore, anisomycin (a p38 MAPK activator) abolished the protective effect of rhTrx on ox-LDL-stimulated RAW264.7 cells, and SB203580 (a p38 MAPK inhibitor) exerted a similar effect as rhTrx. Collectively, these findings indicate that rhTrx suppresses ox-LDL-stimulated foam cell formation and macrophage apoptosis by inhibiting ROS generation, p38 MAPK activation and LOX-1 expression. Therefore, we propose that rhTrx has therapeutic potential in the prevention and treatment of atherosclerosis.

#Thioredoxin-1 #Foam cell #Apoptosis #Atherosclerosis #p38 MAPK

참고문헌 (37)

참고문헌 신청

Chen, G. / 2016 / Thioredoxin-1 increases survival in sepsis by inflammatory response through suppressing endoplasmic reticulum stress / Shock 46:67~74

Cohen, J. I. / 2009 / Exogenous thioredoxin prevents ethanol-induced oxidative damage and apoptosis in mouse liver / Hepatology 49:1709~1717

Cuadrado, A. / 2010 / Mechanisms and functions of p38 MAPK signalling / Biochem. J. 429:403~417

D’Annunzio, V. / 2016 / Role of thioredoxin-1 in ischemic preconditioning, postconditioning and aged ischemic hearts / Pharmacol. Res. 109:24~31

Dai, M. X. / 2014 / The impact of intermittent and repetitive cold stress exposure on endoplasmic reticulum stress and instability of atherosclerotic plaques / Cell. Physiol. Biochem. 34:393~404

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