Effet des nitrites et des nitrates sur les rétines de bœuf in vitro

Hartani, D.; Belguendouz, Houda; Guenane, H.; Chachoua, L.; Lahlou-Boukoffa, O.Q.; Touil-Boukoffa, Chafia

doi:10.1016/s0181-5512(06)73744-5

Cited by 10 publications

(2 citation statements)

References 11 publications

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“…Besides cytokines and chemokines, VEGF, AQP4, GS, NO, NOS, and nestin have been reported to play important roles in inflammation in various tissues under pathological conditions, including the retina [17,19,23,25,26]. NO is a unique gaseous molecule that may act as a chemical messenger involved in vasodilation and neuroinflammation.…”

Section: Resultsmentioning

confidence: 99%

“…As far as can be ascertained, the effects of primary blast injury on the retina have not been reported. In view of this lack of information, we have chosen VEGF, AQP4, GS, iNOS, glutamate, and nestin as the main parameters for investigation as these factors have been reported to be closely linked to inflammation, apoptosis and edema in the brain, spinal cord, and lung after primary blast exposure [9-11,13,16,17,19,21,25,26]. …”

Section: Discussionmentioning

confidence: 99%

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Primary blast injury-induced lesions in the retina of adult rats

Zou

Kan

et al. 2013

J Neuroinflammation

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BackgroundThe effect of primary blast exposure on the brain is widely reported but its effects on the eye remains unclear. Here, we aim to examine the effects of primary blast exposure on the retina.MethodsAdult male Sprague–Dawley rats were exposed to primary blast high and low injury and sacrificed at 24 h, 72 h, and 2 weeks post injury. The retina was subjected to western analysis for vascular endothelial growth factor (VEGF), aquaporin-4 (AQP4), glutamine synthethase (GS), inducible nitric oxide synthase (NOS), endothelial NOS, neuronal NOS and nestin expression; ELISA analysis for cytokines and chemokines; and immunofluorescence for glial fibrillary acidic protein (GFAP)/VEGF, GFAP/AQP4, GFAP/nestin, GS/AQP4, lectin/iNOS, and TUNEL.ResultsThe retina showed a blast severity-dependent increase in VEGF, iNOS, eNOS, nNOS, and nestin expression with corresponding increases in inflammatory cytokines and chemokines. There was also increased AQP4 expression and retinal thickness after primary blast exposure that was severity-dependent. Finally, a significant increase in TUNEL+ and Caspase-3+ cells was observed. These changes were observed at 24 h post-injury and sustained up to 2 weeks post injury.ConclusionsPrimary blast resulted in severity-dependent pathological changes in the retina, manifested by the increased expression of a variety of proteins involved in inflammation, edema, and apoptosis. These changes were observed immediately after blast exposure and sustained up to 2 weeks suggesting acute and chronic injury mechanisms. These changes were most obvious in the astrocytes and Müller cells and suggest important roles for these cells in retina pathophysiology after blast.

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