Inhibition of nNOS and COX-2 expression by lutein in acute retinal ischemia

Choi, Jun-Sub; Kim, Dongmyung; Hong, Yeon-Mi; Mizuno, Satoshi; Joo, Choun‐Ki

doi:10.1016/j.nut.2005.08.011

Cited by 28 publications

(43 citation statements)

References 22 publications

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“…Moreover, like diabetic retinopathy, retinopathy induced by I/R causes up-regulation of NOS2, COX-2, and IL-1 (39,44,46), and therapeutic approaches that inhibit development of diabetic retinopathy in animals (blockade or inhibition of the expression of NOS2, TNF-␣, and IL-1) likewise inhibit the retinal pathology after I/R (7,39,44,46,47). These overlapping features between diabetic and I/R-induced retinopathies raise the possibility that CD40 is a mediator also of diabetic retinopathy.…”

Section: Discussionmentioning

confidence: 99%

CD40 Mediates Retinal Inflammation and Neurovascular Degeneration

Portillo

Grol

Zheng

et al. 2008

The Journal of Immunology

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Retinopathies are major causes of visual impairment. We used a model of ischemic retinopathy to examine the role of CD40 in the pathogenesis of retinal injury. Retinal inflammation, loss of ganglion cells, and capillary degeneration were markedly attenuated in ischemic retinas of CD40−/− mice. Up-regulation of NOS2 and COX2 after retinal ischemia were blunted in CD40−/− mice. NOS2-COX-2 up-regulation in ischemic retinas from wild-type mice was at least in part explained by recruitment of NOS2+COX-2+ leukocytes. Up-regulation of KC/CXCL1 and ICAM-1 also required CD40. Retinal endothelial and Muller cells expressed CD40. Stimulation of these cells through CD40 caused ICAM-1 up-regulation and KC/CXCL1 production. Bone marrow transplant experiments revealed that leukocyte infiltration, ganglion cell loss, and up-regulation of proinflammatory molecules after retinal ischemia were dependent on CD40 expression in the retina and not peripheral blood leukocytes. These studies identified CD40 as a regulator of retinal inflammation and neurovascular degeneration. They support a model in which CD40 stimulation of endothelial and Muller cells triggers adhesion molecule up-regulation and chemokine production, promoting the recruitment of leukocytes that express NOS2/COX-2, molecules linked to neurovascular degeneration.

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Section: Discussionmentioning

confidence: 99%

CD40 Mediates Retinal Inflammation and Neurovascular Degeneration

Portillo

Grol

Zheng

et al. 2008

The Journal of Immunology

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“…Importantly, a significant reduction in lipid peroxidation by L has been demonstrated in vivo for newborn infants, who are at substantial risk of oxidative stress, given the intense metabolic nature of development and low stores of diet-based antioxidants [46,47]. Moreover, L has been found to have meaningful anti-inflammatory action [48,49], which could serve to modulate the many negative effects of inflammation associated not only with injury and disease, but also that brought on by psychological stress [50]. …”

Section: Lutein and Nitric Oxide: A Homeostatic Symbiosismentioning

confidence: 99%

Nitric Oxide and Lutein: Function, Performance, and Protection of Neural Tissue

Stringham

2015

Foods

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The soluble gas neurotransmitter nitric oxide (NO) serves many important metabolic and neuroregulatory functions in the retina and brain. Although it is necessary for normal neural function, NO can play a significant role in neurotoxicity. This is often seen in disease states that involve oxidative stress and inflammation of neural tissues, such as age-related macular degeneration and Alzheimer’s disease. The dietary xanthophyll carotenoid lutein (L) is a potent antioxidant and anti-inflammatory agent that, if consumed in sufficient amounts, is deposited in neural tissues that require substantial metabolic demand. Some of these specific tissues, such as the central retina and frontal lobes of the brain, are impacted by age-related diseases such as those noted above. The conspicuous correspondence between metabolic demand, NO, and L is suggestive of a homeostatic relationship that serves to facilitate normal function, enhance performance, and protect vulnerable neural tissues. The purpose of this paper is to review the literature on these points.

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“…4 It is relevant that perinatal inflammation, often caused or exacerbated by oxidative stress, features in the pathogenesis of common diseases of prematurity. [5][6][7] Several investigators have suggested dietary carotenoids might enhance retinal function in infants [8][9][10][11] and protect against inflammation and oxidative damage. [12][13][14][15][16] However, research into this important subject in neonatal nutrition is limited.…”

Section: Introductionmentioning

confidence: 99%

Effect of carotenoid supplementation on plasma carotenoids, inflammation and visual development in preterm infants

et al. 2011

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Objective: Dietary carotenoids (lutein, lycopene and b-carotene) may be important in preventing or ameliorating prematurity complications. Little is known about carotenoid status or effects of supplementation.Study Design: This randomized controlled multicenter trial compared plasma carotenoid levels among preterm infants (n ¼ 203, <33 weeks gestational age) fed diets with and without added lutein, lycopene and b-carotene with human milk (HM)-fed term infants. We assessed safety and health.Result: Plasma carotenoid levels were higher in the supplemented group at all time points (P<0.0001) and were similar to those of term HM-fed infants. Supplemented infants had lower plasma C-reactive protein (P<0.001). Plasma lutein levels correlated with the full field electroretinogram-saturated response amplitude in rod photoreceptors (r ¼ 0.361, P ¼ 0.05). The supplemented group also showed greater rod photoreceptor sensitivity (least squares means 6.1 vs 4.1; P<0.05). Conclusion:Carotenoid supplementation for preterm infants raises plasma concentrations to those observed in HM-fed term infants. Carotenoid supplementation may decrease inflammation. Our results point to protective effects of lutein on preterm retina health and maturation.

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Inhibition of nNOS and COX-2 expression by lutein in acute retinal ischemia

Cited by 28 publications

References 22 publications

CD40 Mediates Retinal Inflammation and Neurovascular Degeneration

CD40 Mediates Retinal Inflammation and Neurovascular Degeneration

Nitric Oxide and Lutein: Function, Performance, and Protection of Neural Tissue

Effect of carotenoid supplementation on plasma carotenoids, inflammation and visual development in preterm infants

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