Chamomile: An anti-inflammatory agent inhibits inducible nitric oxide synthase expression by blocking RelA/p65 activity

被引:93
作者
Bhaskaran, Natarajan
Shukla, Sanjeev
Srivastava, Janmejai K. [3 ]
Gupta, Sanjay [1 ,2 ]
机构
[1] Case Western Reserve Univ, Dept Urol, Univ Hosp Case Med Ctr, Cleveland, OH 44106 USA
[2] Case Comprehens Canc Ctr, Cleveland, OH 44106 USA
[3] Amity Univ, Inst Biotechnol, Lucknow, Uttar Pradesh, India
关键词
inflammation; nitric oxide; chamomile; nuclear factor-kappa B; macrophages; pro-inflammatory cytokines; NF-KAPPA-B; MATRICARIA-RECUTITA L; MACROPHAGE ACTIVATION; RAW-264.7; MACROPHAGES; COX-2; EXPRESSION; P65; SUBUNIT; LIPOPOLYSACCHARIDE; CELLS; SUPPRESSION; INDUCTION;
D O I
10.3892/ijmm_00000545
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
100103 [病原生物学]; 100218 [急诊医学];
摘要
Chamomile has long been used in traditional medicine for the treatment of inflammation-related disorders. In this study we investigated the inhibitory effects of chamomile on nitric oxide (NO) production and inducible nitric oxide synthase (iNOS) expression, and explored its potential anti-inflammatory mechanisms using RAW 264.7 macrophages. Chamomile treatment inhibited LPS-induced NO production and significantly blocked IL-1 beta, IL-6 and TNF alpha-induced NO levels in RAW 264.7 macrophages. Chamomile caused reduction in LPS-induced iNOS mRNA and protein expression. In RAW 264.7 macrophages, LPS-induced DNA binding activity of RelA/p65 was significantly inhibited by chamomile, an effect that was mediated through the inhibition of IKK beta, the upstream kinase regulating NF-kappa B/Rel activity, and degradation of inhibitory factor-kappa B. These results demonstrate that chamomile inhibits NO production and iNOS gene expression by inhibiting RelA/p65 activation and supports the utilization of chamomile as an effective anti-inflammatory agent.
引用
收藏
页码:935 / 940
页数:6
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