Objective To observe the effect of celecoxib on the expression vascular endothelial growth factors (VEGF) in diabetic rats. Methods Thirty-six wistar rats were used to establish the diabetic models by intraperitoneal injection with streptozotocin. The diabetic rats were divided into 2 groups: diabetic group (n=18) and celecoxib group (n=18). Celecoxib (50 mg/kg) was administered orally to the rats in celecoxib group and the physiological saline with the same volume was given orally to the rats in diabetic group. Eighteen else rats were in normal control group. All of the rats were executed 3 months later. The expression of VEGF protein was detected by immunohistochemistry method. Reverse transcription-polymerase chain reaction（RT-PCR） analysis was used to examine the expression of retinal VEGF mRNA and cyclooxygenase-2 mRNA. Results Lower positive expression of VEGF mRNA and cyclooxygenase-2 mRNA, weakly positive action of immunohistochemistry of VEGF, and lower expression of VEGF protein were detected in normal control group; in the diabetic group, the expression of VEGF mRNA and cyclooxygenase-2 mRNA increased obviously comparing with which in the control group (Plt;0.05), and the bly positive action of immunohistochemistry of VEGF and increased expression of VEGF protein were detected (Plt;0.01); in celecoxib group, the expression of VEGF mRNA was lower than that in the diabetic group (Plt;0.05), the expression of cyclooxygenase-2 mRNA didnprime;t decrease much (Pgt;0.05), the positive action of immunohistochemistry of VEGF decreased, and the expression of VEGF protein decreased (Plt;0.01). Conclusion By inhibiting the activation of cyclooxygenase-2, celecoxib can inhibit the expression of retinal VEGF mRNA and protein in diabetic rats induced by streptozotocin. (Chin J Ocul Fundus Dis,2007,23:265-268)
Objective To observe the changes of expression of glutamine synthetase (GS) in early diabetic ratsprime; retina and investigate its possible mechanism. Methods Three groups of streptozotocininduced diabetic models of SpragueDawley (SD) rats with different diseased courses, ie, 1 month, 2 months, and 3 months, respectively, with 8 rats in each group, and 8 normal ones as control were examined. The expressions of GS, interleukin-1beta; (IL-1beta;) and c-Jun in retina in the 4 groups were detected by indirect immunofluorescence and western blotting techniques. Meanwhile, different doses of IL-1beta;（0,100,500,and 1000 ng/ml） were injected into the vitreous cavities of 32 normal rats (8 rats in each group), and 24 hours later, the expressions of GS and c-Jun in retina were detected by the same methods. Results The expression of GS in retina did not changed in control group or in 1 month and 2 months group, but decreased obviously in 3 months group comparing with which in the control group (Plt;0.01).The expressions of c-Jun and IL-1beta; in retina in control group were very low, but increased gradually in diabetic rats in 1-3 months group, which significantly differed from which in the control group (Plt;0.01). Vitreous injection with IL-1beta; (500 and 1000 ng/ml) down regulated the expressions of GS, and the expression of c-Jun increased in a dose-dependent way after injection with IL-1beta; at the concentration of 100 ng/ml. Conclusions In early diabetic ratsrsquo; retina, IL-1beta; may down regulate the expression of GS. The possible mechanism may be the activation of c-Jun by IL-1beta;. (Chin J Ocul Fundus Dis,2007,23:260-264)
Objective To investigate the effect of intravitreal injection with dexamethasone on leukocyte accumulation, vascular permeability, and the expression of intercellular adhension molecule (ICAM-1) in rats with diabetes. Methods Seventy-two BN rats were divided into 4 groups: control group, diabetes group, diabetes+ physiologic saline group, and diabetes+ dexamethasone group, with 18 rats in each group. Streptozotocin was injected into the rats to set up the diabetic model. Accumulated leukocytes were counted in vivo by acridine orange leukocyte fluorography, and retinal vascular permeability was measured by Evans blue assay. The expression of mRNA and protein level of ICAM-1 were evaluated by real-time quantitative polymerase chain reaction analysis and enzymelinked immunosorbent assay. Results In the diabetes+ dexamethasone group, accumulated leukocytes were reduced, retinal vascular permeability decreased, and the expression of ICAM-1 decreased. The expression of ICAM-1 mRNA and protein levels in control group, diabetes group, diabetes+ physiologic saline group, and diabetes+ dexamethasone group were 0.43plusmn;0.07，0.76plusmn;0.21，0.74plusmn;0.18，and 0.55plusmn;0.13; (37.90plusmn;4.56), (76.74plusmn;6.68), (74.32plusmn;7.11), and (39.61plusmn;4.47) pg/mg respectively. Conclusions Dexamethasone can reduce accumulated leukocytes and retinal vascular permeability, which may be caused by inhibiting the expression of ICAM-1. (Chin J Ocul Fundus Dis,2007,23:273-276)
Objective To observe the expression of N-cadherin in streptozotocin (STZ)-induced diabetic Sprague-Dawley (SD) ratsprime;retinae. Methods Celiac injection with 65 mg/kg STZ was performed on 20 rats to set up the diabetic model, and celiac injection with the same volume citrate buffer was performed on other 20 SD rats as the control. Vascular permeability was detected by Evans blue method. The expression of N-cadherin in both normal and STZ-induced diabetic ratsprime;retinae and trypsinase-digested retinal microvessels were detected by immunohistochemistry method and Western blotting analysis. Results Retinal vascular permeability increased 68%, 91% and 125% 4, 8, and 12 weeks, respectively, after diabetic models was induced (Plt;0.005). In the control group, the expression of N-cadherin was detected in the outer and inner plexiform layer, inner nuclear layer，ganglion cell layer,internal limiting membrane and between retinal endothelial cells and pericytes. However, the expression of N-cadherin significantly decreased in STZ-induced diabetic rats retinae at the 12th week. The results of Western blotting analysis showed that the expression of N-cadherin obviously decreased as the diabetic retinopathy developed. Conclusion The decrease of expression of Ncadherin in the retinae of STZ-induced diabetic rats suggests that N-cadherin may participate in the development of diabetic retinopathy at the early stage. (Chin J Ocul Fundus Dis,2007,23:269-272)