Experimental model of acute ischemia of the retina in rats

Kalamkarov, G. R.; Цапенко, И. В.; Mv, Zueva; Иванов, А. Н.; Konstantinova, T. S.; Бугрова, А. Е.; Rezvykh, S. V.; Федоров, А. А.; Shevchenko, T. F.

doi:10.1007/s10517-008-0174-7

Cited by 12 publications

(4 citation statements)

References 5 publications

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“…49 Reduction of b/a ratio is another sensitive prognostic sign for ischemic injury in an animal model of retinal ischemia and in human central retinal vein occlusion. [43][44][45][46] In the present study, no obvious reduction of a-wave was noted in the vehicletreated animals, indicating no considerable functional deficiency in photoreceptors in our retinal I/R model. This correlated with our previous findings that no apoptotic nucleus was found in the outer retinal layer after ischemic injury.…”

Section: Discussionsupporting

confidence: 40%

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Anti-Inflammatory Effects of Lutein in Retinal Ischemic/Hypoxic Injury: In Vivo and In Vitro Studies

Fung

et al. 2012

Invest. Ophthalmol. Vis. Sci.

118

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PURPOSE. Lutein protects retinal neurons by its anti-oxidative and anti-apoptotic properties in ischemia/reperfusion (I/R) injury while its anti-inflammatory effects remain unknown. As Müller cells play a critical role in retinal inflammation, the effect of lutein on Müller cells was investigated in a murine model of I/R injury and a culture model of hypoxic damage.METHODS. Unilateral retinal I/R was induced by a blockade of internal carotid artery using the intraluminal method in mice. Ischemia was maintained for 2 hours followed by 22 hours of reperfusion, during which either lutein (0.2 mg/kg) or vehicle was administered. Flash electroretinogram (flash ERG) and glial fibrillary acidic protein (GFAP) activation were assessed. Lutein's effect on Müller cells was further evaluated in immortalized rat Müller cells (rMC-1) challenged with cobalt chloride-induced hypoxia. Levels of IL-1b, cyclooxygenase-2 (Cox-2), TNFa, and nuclear factor-NF-kappa-B (NF-jB) were examined by Western blot analysis. RESULTS.Lutein treatment minimized deterioration of b-wave/awave ratio and oscillatory potentials as well as inhibited upregulation of GFAP in retinal I/R injury. In cultured Müller cells, lutein treatment increased cell viability and reduced level of nuclear NF-jB, IL-1b, and Cox-2, but not TNFa after hypoxic injury.CONCLUSIONS. Reduced gliosis in I/R retina was observed with lutein treatment, which may contribute to preserved retinal function. Less production of pro-inflammatory factors from Müller cells suggested an anti-inflammatory role of lutein in retinal ischemic/hypoxic injury. Together with our previous studies, our results suggest that lutein protected the retina from ischemic/hypoxic damage by its anti-oxidative, antiapoptotic, and anti-inflammatory properties. (Invest Ophthalmol Vis Sci. 2012;53:5976-5984)

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Section: Discussionsupporting

confidence: 40%

“…In addition, the ratio of b-wave/a-wave amplitude (b/a ratio) was also estimated as it is one of the sensitive parameters to evaluate the functional changes in retinal injury. [43][44][45][46] The amplitudes of awave in all animal group did not show any noticeable difference ( Fig. 1B; P > 0.05).…”

Section: Functional Analysis Using Electroretinogrammentioning

confidence: 81%

Anti-Inflammatory Effects of Lutein in Retinal Ischemic/Hypoxic Injury: In Vivo and In Vitro Studies

Fung

et al. 2012

Invest. Ophthalmol. Vis. Sci.

118

View full text Add to dashboard Cite

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“…Visual dysfunction caused by retinal degeneration, measured noninvasively by electroretinogram (ERG), showed an obvious reduction in the ERG response generated at the post-receptor level of the inner retina [50,51]. In a rodent model of ischemic glaucomatous injury, a functional impairment was indicated by a significantly smaller oscillatory potential amplitude and b-wave/a-wave ratio [50], the latter being a sensitive prognostic measure of ischemic injury in both animal models and humans [233][234][235][236]. Similar results were seen in NMDA-induced RGC injury, showing a significant reduction in the amplitude of the photopic negative response, which implied a post-receptor impairment [51].…”

Section: Carotenoids In the Management Of Glaucoma (Preclinical Studies)mentioning

confidence: 99%

Carotenoids in the Management of Glaucoma: A Systematic Review of the Evidence

Lem

Gierhart²,

Davey

2021

Nutrients

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Primary open-angle glaucoma (POAG) remains a leading cause of irreversible blindness globally. Recent evidence further substantiates sustained oxidative stress, and compromised antioxidant defenses are key drivers in the onset of glaucomatous neurodegeneration. Overwhelming oxidative injury is likely attributed to compounding mitochondrial dysfunction that worsens with age-related processes, causing aberrant formation of free radical species. Thus, a compromised systemic antioxidant capacity exacerbates further oxidative insult in glaucoma, leading to apoptosis, neuroinflammation, and subsequent tissue injury. The purpose of this systematic review is to investigate the neuroprotective benefits of the macular carotenoids lutein, zeaxanthin, and meso-zeaxanthin on glaucomatous neurodegeneration for the purpose of adjunctive nutraceutical treatment in glaucoma. A comprehensive literature search was conducted in three databases (PubMed, Cochrane Library, and Web of Science) and 20 records were identified for screening. Lutein demonstrated enhanced neuroprotection on retinal ganglion cell survival and preserved synaptic activity. In clinical studies, a protective trend was seen with greater dietary consumption of carotenoids and risk of glaucoma, while greater carotenoid levels in macular pigment were largely associated with improved visual performance in glaucomatous eyes. The data suggest that carotenoid vitamin therapy exerts synergic neuroprotective benefits and has the capacity to serve adjunctive therapy in the management of glaucoma.

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“…The hepatic vein blood ammonia level depends linearly on a portal ammonia level [19], and the latter on a luminal ammonia concentration [16]. The caval blood ammonia level may have the similar dependence because of the substantial rate of the transperitoneal ammonia translocation [20]. Hence, the flux of gastrointestinal ammonia into the common bloodstream and then into the brain may vary depending on the digestive tract luminal ammonia pool.…”

Section: Discussionmentioning

confidence: 99%

Promotion of the Toxic Action of Cyclophosphamide by Digestive Tract Luminal Ammonia in Rats

2011

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To estimate the influence of the digestive tract luminal ammonia pool on acute toxic effects of cyclophosphamide, the dynamics of blood ammonia, glutamine and urea level, symptoms of toxic action and the survival time have been studied in rats, intraperitoneally treated with cyclophosphamide, at the background of the gavage with non-lethal dose of ammonium acetate (12 mmol/kg, i.e., 0.35 LD50). Ammonium acetate enhanced the hyperammonaemic action of cyclophosphamide while promoting its lethal action: the mean survival time decreased 1.5, 2.1, 2.8, or 6.1 times at the background of cyclophosphamide i/p doses 200, 600, 1000, or 1400 mg/kg, respectively. Animals exposed to the combination of toxicants, manifested symptoms which were characteristic of the effect of lethal doses of ammonia salts. These data provide the evidence of the detrimental role of gastrointestinal luminal ammonia in the acute high-dose cyclophosphamide toxicity.

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Experimental model of acute ischemia of the retina in rats

Cited by 12 publications

References 5 publications

Anti-Inflammatory Effects of Lutein in Retinal Ischemic/Hypoxic Injury: In Vivo and In Vitro Studies

Anti-Inflammatory Effects of Lutein in Retinal Ischemic/Hypoxic Injury: In Vivo and In Vitro Studies

Carotenoids in the Management of Glaucoma: A Systematic Review of the Evidence

Promotion of the Toxic Action of Cyclophosphamide by Digestive Tract Luminal Ammonia in Rats

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