Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.6.3.1 (NADPH oxidase)
 11,281 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

LIGHT acted as a new player in the atherogenesis. The dried, unripe fruit of Evodia Fructus (EF) has long been used as a traditional Chinese herbal medicine, and is currently widely used for the treatment of headache, abdominal pain, vomiting, colds and reduced blood circulation. Evodiamine and rutaecarpine are active components of EF. In this study, we investigated the inhibitory effect of evodiamine and rutaecarpine on LIGHT-induced migration in human monocytes. Evodiamine and rutaecarpine decreased the LIGHT-induced production of ROS, IL-8, monocyte chemoattractant protein-1 (MCP-1), TNF-alpha, and IL-6, as well as the expression of chemokine receptor (CCR) 1, CCR2 and ICAM-1 and the phosphorylation of the ERK 1/2 and p38 MAPK. Furthermore, NADPH oxidase assembly inhibitor, AEBSF, blocked LIGHT-induced migration and activation of CCR1, CCR2, ICAM-1, and MAPK such as ERK and p38 in a manner similar to evodiamine and rutaecarpine. These findings indicate that the inhibitory effects of evodiamine and rutaecarpine on LIGHT-induced migration and the activation of CCR1, CCR2, ICAM-1, ERK, and p38 MAPK occurs via decreased ROS production and NADPH oxidase activation. Taken together, these results indicate that evodiamine and rutaecarpine have the potential for use as an anti-atherosclerosis agent.
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PMID:Evodiamine and rutaecarpine inhibit migration by LIGHT via suppression of NADPH oxidase activation. 1924 41

LIGHT is known to act as a novel mediator for atherogenesis. Furthermore, it has been reported that emodin, an active component extracted from rhubarb, can stop the growth of cancer cells. However, it is not known if emodin exerts anti-atherogenic effects in the human monocyte, THP-1, following treatment with LIGHT. In this study, we evaluated the inhibitory effect of emodin and rhein on LIGHT-induced migration in THP-1. Emodin and rhein decreased the level of LIGHT-induced generation of ROS, as well as the expression of CCR1, CCR2 and ICAM-1 and the production of IL-8, MCP-1, TNF-alpha, and IL-6. Emodin and rhein also decreased the phosphorylation of the p38 MAPK and IkB-alpha. Furthermore, the NADPH oxidase assembly inhibitor, AEBSF, and the blocker of NADPH oxidase, p47(phox) small interference RNA (siRNA), also efficiently blocked LIGHT-induced migration, CCR1, CCR2, ICAM-1, and HVEM expression, and p38 MAPK and NF-kB activation. These findings indicate that the inhibitory effects of emodin and rhein on LIGHT-induced migration occur via decreasing ROS production and NADPH oxidase p47(phox) activation. Taken together, these results indicate that emodin and rhein have the potential for use as an anti-atherosclerosis agent.
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PMID:Emodin and rhein inhibit LIGHT-induced monocytes migration by blocking of ROS production. 2029 10

Recent studies show that low-level laser therapy (LLLT) has an important anti-inflammatory action in acute lung inflammation. The present work explored if laser therapy is able to antagonize eosinophils and allergic inflammation induced by oxidative stress in Balb/c mice. Forty-eight hours after challenge, the leukocyte counting, ROS and nitrite/nitrate level, RANTES, CCL3, CCL8 as well as eotaxins were measured in the bronchoalveolar lavage fluid (BALF) of laser-treated mice or not. Into the lung, some chemokines receptors, the iNOS activity and mRNA expression, and the activities of superoxide dismutase (SOD), catalase, gluthatione, NADPH oxidase activities and thiobarbituric acid reactive species (T-Bars) were measured. Laser-treated allergic mice presented reduction of both the ICAM-1 and eosinophil in the lungs. RANTES, CCL8, CCL3 and eotaxins were reduced in BALF of laser-treated allergic mice. In allergic mice lung LLLT decreased the CCR1 and CCR3 and restored the oxidative stress balance as well. Laser decreased the lipidic peroxidation in allergic mice lung as much as increased SOD, GPx and GR. It shows that LLLT on allergic lung inflammation involves leukocyte-attractant chemokines and endogenous antioxidant. Based on results, LLLT may ultimately become a non- invasive option in allergic lung disease treatment. The top figure illustrates the laser decreasing the eosinophils migration into BALF and the bottom figure shows the laser upregulating the expression of heme-oxygenase (anti-oxidant enzyme) in lung tissue anti-oxidant.
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PMID:The chemokines secretion and the oxidative stress are targets of low-level laser therapy in allergic lung inflammation. 2764 82