期刊
FREE RADICAL BIOLOGY AND MEDICINE
卷 48, 期 10, 页码 1423-1434出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.freeradbiomed.2010.02.031
关键词
Benfotiamine; Vitamin B1; Oxidative stress; NF-kappa B; Macrophages; Inflammation; Free radicals
资金
- NIH [GM71036, EY018591, DK36118]
- NIEHS Core Facility [ES-006676]
This study was designed to investigate the molecular mechanisms by which benfotiamine, a lipid-soluble analogue of vitamin B1, affects lipopolysaccharide (LPS)-induced inflammatory signals leading to cytotoxicity in the mouse macrophage cell line RAW264.7. Benfotiamine prevented LPS-induced apoptosis, expression of the Bcl-2 family of proapoptotic proteins, caspase-3 activation, and PARP cleavage and altered mitochondrial membrane potential and release of cytochrome c and apoptosis-inducing factor and phosphorylation and subsequent activation of p38-MAPK, stress-activated kinases (SAPK/JNK), protein kinase C, and cytoplasmic phospholipase A2 in RAW cells. Further, phosphorylation and degradation of inhibitory kappa B and consequent activation and nuclear translocation of the redox-sensitive transcription factor NF-kappa B were significantly prevented by benfotiamine. The LPS-induced increased expression of cytokines and chemokines and the inflammatory marker proteins iNOS and COX-2 and their metabolic products NO and PGE(2) was also blocked significantly. Thus, our results elucidate the molecular mechanism of the anti-inflammatory action of benfotiamine in LPS-induced inflammation in murine macrophages. Benfotiamine suppresses oxidative stress-induced NF-kappa B activation and prevents bacterial endotoxin-induced inflammation, indicating that vitamin 61 supplementation could be beneficial in the treatment of inflammatory diseases. (C) 2010 Elsevier Inc. All rights reserved.
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