More and more people suffered from the car otid artery obstruction. It is reported that it's around 69% of these patients the first clinical manifes tation of carotid occlusive disease is the ocular ischemic syndrome. Owing to th e most symptoms of the ocular ischemic syndrome are very obscure, so there are a lways overlook or made a misdiagnosis of this entity in clinical. Fundus fluores cein angiography (FFA) is the best procedure to find this entity. We should pay close attention to notice the early phase of FFA. It is the most specific FFA si gn in ocular ischemic syndrome, and it is a distinctly unusual finding to find t he ocular ischemic syndrome. (Chin J Ocul Fundus Dis, 2008, 24: 79-81)
ObjectiveTo investigate the relationship between the pathological and functional changes of the retina and the expression of monocyte chemoattractant protein (MCP)-1 after retinal laser injury in mice. MethodsA total of 116 C57BL/6 mice were randomly divided into the normal group (58 mice) and the injured group (58 mice). Retinal laser injuries were induced by Argon ion laser. At 1, 3, 7 days after laser injury, electroretinogram (ERG) responses were recorded to detect the function of the retina. Hematoxylin and eosin (HE) staining was performed to observe pathological changes. Quantitative real-time polymerase chain reaction (PCR) was performed to detect gene expression of MCP-1. Western blot was used to measure the protein expression of MCP-1. ResultsHE staining showed a progressive damage of the retinal structure. The results of ERG showed that the differences of dark-adaptive a wave (t=6.998, 9.594, 13.778) and b wave (t=12.089, 13.310, 21.989) amplitudes of 1, 3 and 7 day post-injury between normal group and injured group were statistically significant (P=0.000). At 1 day post-injury, the differences of light adaptive b wave amplitudes between the two groups were statistically significant (t=8.844, P=0.000). While the differences of light-adaptive a wave amplitudes were not (t=2.659,P=0.200). At 3, 7 days post-injury, the differences of a (t=3.076, 7.544) and b wave amplitudes (t=10.418, 8.485) between the two groups were statistically significant (P=0.000). In dark-adaptive ERG, the differences of a wave amplitudes between 1 day and 3 days (t=3.773), 1 day and 7 days (t=5.070) and b wave amplitudes between 1 day and 7 days (t=4.762) were statistically significant (P<0.01), while the differences of a wave amplitudes between the 3 days and 7 days (t=1.297) and b wave amplitudes between 1 day and 3 days (t=2.236), 3 day and 7 days (t=2.526) were not significant (P=0.660, 0.120, 0.060). In light-adaptive ERG, the differences of a wave amplitudes between 1 day and 7 days (t=2.992) and b wave amplitudes between 1 day and 3 days (t=3.570), 1day and 7 days (t=4.989) were statistically significant (P<0.05), while the differences of a wave amplitudes between 1 day and 3 days (t=0.516), the 3 days and 7 days (t=2.475) and b wave amplitudes between 3 days and 7 days (t=1.419) were not significant (P=1.000, 0.710, 0.070). Quantitative real-time PCR showed that the differences of MCP-1 gene expression at 1, 3 and 7 day post-injury between normal group and injured group were statistically significant (t=14.329, 16.861, 5.743; P<0.05). Western blot showed that the differences of MCP-1 protein expression at 1, 3 and 7 day post-injury between normal group and injured group were statistically significant (t=75.068, 54.145, 14.653; P<0.05). ConclusionIn the first 7 days after mice retinal laser injury, there are progressive pathological and functional damage of the retina, which might be correlated with MCP-1 expression.
Monocyte chemoattractant protein-1(MCP-1) is a cytokine which belongs to the CC chemokine family. Retinal pigment epithelium (RPE) cells, photoreceptors and microglial cells in the retina can secrete MCP-1. Physiological level of MCP-1 is important for preserving morphology of RPE and glial cells, as well as retinal function and gross morphology. MCP-1 is likely released from Müller glia and the RPE cells when retina under stress, and attracts microglia/macrophages to the sites of retinal damage, activates the microglia to ingest cell debris. MCP-1 has been found upregulated in the intraocular fluid of retina in patients and animal models with retinal detachment, posterior uveitis and age-related macular degeneration. The expression of MCP-1 may be response to retinal inflammation. Therefore, it is tempting to speculate that pharmacological targeting of MCP-1 may be a safe and viable strategy in treatment of retinal disease.