Direct, real-time, simultaneous monitoring of intravitreal nitric oxide and oxygen in endotoxin-induced uveitis in rabbits

Yomura, Y.; Shoji, Yasuhiro; Asai, Daisuke; Murakami, Eiichi; Ueno, Satoki; Nakashima, Hideki

doi:10.1016/j.lfs.2007.01.021

Cited by 16 publications

(9 citation statements)

References 34 publications

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“…The partial pressure of oxygen (pO 2 ) in the calf muscles was measured using an electrode 37 . The rat was held on the platform immediately after injury.…”

Section: Methodsmentioning

confidence: 99%

Hyperbaric oxygen reduces inflammation, oxygenates injured muscle, and regenerates skeletal muscle via macrophage and satellite cell activation

Oyaizu

Enomoto

Yamamoto

et al. 2018

Sci Rep

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Hyperbaric oxygen treatment (HBO) promotes rapid recovery from soft tissue injuries. However, the healing mechanism is unclear. Here we assessed the effects of HBO on contused calf muscles in a rat skeletal muscle injury model. An experimental HBO chamber was developed and rats were treated with 100% oxygen, 2.5 atmospheres absolute for 2 h/day after injury. HBO reduced early lower limb volume and muscle wet weight in contused muscles, and promoted muscle isometric strength 7 days after injury. HBO suppressed the elevation of circulating macrophages in the acute phase and then accelerated macrophage invasion into the contused muscle. This environment also increased the number of proliferating and differentiating satellite cells and the amount of regenerated muscle fibers. In the early phase after injury, HBO stimulated the IL-6/STAT3 pathway in contused muscles. Our results demonstrate that HBO has a dual role in decreasing inflammation and accelerating myogenesis in muscle contusion injuries.

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“…The partial pressure of oxygen (pO 2 ) in the calf muscles was measured using an electrode 37 . The rat was held on the platform immediately after injury.…”

Section: Methodsmentioning

confidence: 99%

Hyperbaric oxygen reduces inflammation, oxygenates injured muscle, and regenerates skeletal muscle via macrophage and satellite cell activation

Oyaizu

Enomoto

Yamamoto

et al. 2018

Sci Rep

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“…The concept that over-active arginase causes retinal disease by reducing NO formation may appear paradoxical given that numerous groups have reported increased levels of NO products (nitrate/nitrite and the peroxynitrite biomarker nitrotyrosine) in models of diabetic retinopathy, EIU and OIR [13, 53, 56, 97]. Studies showing NOS gene deletion or treatment with NOS inhibitors decreases peroxynitrite formation and reduces signs of EIU [31] diabetic retinopathy [26, 53, 58, 102] and OIR [13] strongly support the role of nitrative stress in retinopathy.…”

Section: Arginase and Retinopathymentioning

confidence: 99%

Vascular dysfunction in retinopathy—An emerging role for arginase

Caldwell¹,

Zhang²,

Romero³

et al. 2010

Brain Research Bulletin

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Retinal neovascularization is a leading cause of visual disability. Retinal diseases involving neovascularization all follow the same progression, beginning with vascular inflammatory reactions and injury of the vascular endothelium and ending with neovascularization, fibrosis and retinal detachment. Understanding the mechanisms underlying this process is critical to its prevention and treatment. Research using retinopathy models has revealed that the NOX2 NADPH oxidase has a key role in inducing production of reactive oxygen species and angiogenic cytokines and causing vascular inflammatory reactions and neovascularization. This prospective review addresses the potential role of the urea/ornithine pathway enzyme arginase in this process. Studies of peripheral vessels isolated from diabetic animals have shown that increased arginase activity causes vascular endothelial cell dysfunction by decreasing availability of L-arginine to endothelial cell nitric oxide synthase which decreases nitric oxide bioavailability and increases oxidative stress. Increasing arginase activity also increases formation of polyamines and proline, which can induce cell growth and fibrosis. Studies in models of retinopathy show that increases in oxidative stress and signs of vascular inflammation are correlated with increases in arginase activity and arginase 1 expression and that decreasing arginase expression or inhibiting its activity blocks these effects. Furthermore, the induction of arginase during retinopathy is blocked by knocking out NOX2 or inhibiting NADPH oxidase activity. These observations suggest that NADPH oxidase-induced activation of the arginase pathway has a key role in causing retinal vascular dysfunction during retinopathy. Limiting the actions of arginase could provide a new strategy for treating this potentially blinding condition. Vascular inflammatory reactions and ischemic retinopathyCellular inflammation at the blood-microvascular endothelial cell interface is a common feature of retinal diseases characterized by hyperpermeablity and neovascularization. Recent studies in models of ischemic retinopathy suggest that inflammatory reactions play a key role in initiating vascular injury and dysfunction. [2,28,53,98] Various chemokines and cytokines, such as tumor necrosis factor (TNF)-α, interleukin (IL)-6, vascular endothelial cell growth factor (VEGF) and monocyte chemotactic protein (MCP)-1 are upregulated in ischemic retinopathy and have been reported to cause pathologic inflammatory reactions [47,49,50,54, Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. Confl...

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“…11,12 These have been involved in the pathophysiology of ocular inflammation in the anterior segment of the eye and also the retina. [13][14][15] No comparative study has been performed on the effect of adalimumab or infliximab on inflammatory reactions in experimental uveitis. In the present work we studied the acute effects of adalimumab or infliximab in a uveitis experimental model, i.e., the effects of both drugs on cellular infiltration, protein leakage, oxidative stress markers, and levels of cytokines and chemokines in the aqueous humor of the rats.…”

mentioning

confidence: 99%

Comparison of the Acute Effects of anti-TNF-alpha Drugs on a Uveitis Experimental Model

Johnsen-Soriano¹,

Sancho‐Tello

Arnal³

et al. 2010

Ocular Immunology and Inflammation

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Direct, real-time, simultaneous monitoring of intravitreal nitric oxide and oxygen in endotoxin-induced uveitis in rabbits

Cited by 16 publications

References 34 publications

Hyperbaric oxygen reduces inflammation, oxygenates injured muscle, and regenerates skeletal muscle via macrophage and satellite cell activation

Hyperbaric oxygen reduces inflammation, oxygenates injured muscle, and regenerates skeletal muscle via macrophage and satellite cell activation

Vascular dysfunction in retinopathy—An emerging role for arginase

Comparison of the Acute Effects of anti-TNF-alpha Drugs on a Uveitis Experimental Model

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