Boric acid inhibits LPS-induced TNF-α formation through a thiol-dependent mechanism in THP-1 cells
Boric acid inhibits LPS-induced TNF-α formation through a thiol-dependent mechanism in THP-1 cells
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DOI:
10.1016/j.jtemb.2008.03.005
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发表时间:
2008-01-01
影响因子:
3.5
通讯作者:
Zhong, Laifu
中科院分区:
文献类型:
--
作者:
Cao, Jun;Jiang, Liping;Zhong, Laifu
Oxidative stress plays all important role during Inflammatory diseases and antioxidant administration to diminish oxidative stress may arrest inflammatory processes. Boron has been implicated to modulate certain inflammatory mediators and regulate inflammatory processes. Here we investigated the role of the tripeptide glutathione (GSH) in modulating the effects of boric acid (BA) oil lipopolysaccharide (LPS)-induced tumor necrosis factor alpha (TNF-alpha) formation in THP-1 we found that BA had no significant effects on both TNF-alpha production and intracellular GSH monocytes. interestingly, contents. whereas it could inhibit LPS-induced TNF-alpha formation and ameliorated the D,L-buthionine-S,R-sulfoximine (BSO)-induced GSH depletion. Twenty-four hour incubation with BSO induced a decrease of the intracellular GSH and all increase of TNF-alpha. Treatment with N-acctyl-L-cysteine (NAC) did not significantly increase intracellular content of GSH but significantly reduced the secretion of TNF-alpha. BSO-pretreatment for 24 h enhanced the LPS-induced secretion and mRNA expression of TNF-alpha further. BA inhibited LPS-stimulated TNF-alpha formation was also seen after GSH depletion by BSO. These results indicate that BA may have anti-inflammatory effect in the LPS-stimulated inflammation and the effect of BA on TNF-alpha secretion may be induced via a thiol-dependent mechanism. (C) 2008 Elsevier GmbH. All rights reserved.