RESUMEN
BackgroundResearch demonstrated that vitamin D3 mediated by its receptor has the potent nonclassical effects,including immunomodulatory,antiinflammatory,and neuroprotective properties,and it can enhance the secretion and sensitivity of insulin and therefore down-regulate hyperglycemia and attenuate the corneal edema.ObjectiveThe present study was to investigate the protective effect of vitamin D3on ocular structure in experimental diabetic rat.Methods Twenty-two healthy SPF C57BL/6 rats were randomly divided into vitamine D3 group (8 rabbits),diabetic control group ( 11 rabbits) and normal control group ( 3 rabbits).2％ streptozotocin ( STZ,175 mg/kg)was intraperitoneally injected to create the diabetic models in the rats of the vitamine D3 group and diabetic control group.Blood glucose was examined for 3 times in the third day after STZ injection,and the rats with the blood glucose concentration ＞16.7 mmol/L was identified as the successful diabetic models.After modeling,the rat tail blood was collected for the monitoring of blood glucose.Two weeks after modeling,vitamine D3 was intraperitoneally injected in each week for 5 times.The fundus was examined using direct ophtalmoscope,and the eyeballs were obtained under the excessive anesthesia for the measurement of thickness of the central cornea,retina and choroids by histopathological examination once a week for 7 weeks after administration of vitamin D3.The administration of the animals complied with the Statement of ARVO.ResultsThe corneal edema appeared with the corneal thickness of (339.14± 11.13) μm in the first week and gradually attenuated with time elapse after modeling in the diabetic group ( F =382.446,P =0.000).The corneal thickness values were significantly decreased from the second week through the seventh week in the vitamin D3 group compared with diabetic control group(P＜0.05).The atrophy of the corneal epithelium was found from the fifth week to the seventh week in diabetic control group,but that in vitamin D3 group was slight (P＜0.05).The gradually thinning of the choroids was seen from the first week to the seventh week in the diabetic control group ( F =437.411,P =0.000 ),however,the thickness values in the vitamin D3 group were significantly increased in comparison with the diabetic control group in various time points (P＜0.05).The retina thickness was gradually reduced during the seven-week duration in the diabetic control group (F =91.859,P =0.000),but no significant change was identified in retina thickness in the vitamin D3 group(P＞0.05).ConclusionsVitamin D3 has prevent and therapeutic effects on experimental diabetic oculopathy.
RESUMEN
Background In vitro study showed that chemotaxis consist of chemotaxis factor 4(CXCR4)and stromal cells derived factor-1(SDF-1)and may play a role in the orientation and migration of retinal progenitor cells (RPCs)toward lesion.Overexpression of CXCR4 in RPCs can enhance the chemotaxis activity.Objective This work was to explore the feasibility and underlying mechanism of up-regulation of CXCR4 on RPCs induced by hypoxia.Methods RPCs were retained in an incubator with normal O2volume(16％)or hypoxia condition(10％ O2)for 12 hours and 24 hours respectively.Flow cytometer cell analysis screening(FACS)was conduced to measure the proportion of CXCR4-expressing cells,and CXCR4,HIF-1 mRNA were analyzed by reverse transcription-polymerse chain reaction(RT-PCR).The chemotical effect of 30 mg/L SDF-1 to RPCs cultured under the hypoxia condition was assessed using Boyden chamber.Results The expression level of CXCR4(CXCR4 mRNA/β-actin mRNA)inRPCs cultured by 10％ O2 for 12 and 24 hours were 0.28+0.07and 0.48+0.17 and increased by 1.75 and 3.00 fold more than that of 16％ O2 culture group(0.16+0.02)(P＜0.01).The expression level of HIF-1 mRNA(HIF-1 mRNA/β-actin mRNA)in RPCs cultured by 10％ O2 for 12 and 24 hours were 0.18 ±0.07and 0.38 ±0.13 and increased by 3.00 and 6.30 fold more than that of 16％ O2 culture group(0.06±0.01)(P＜0.01).The chemotical effect of 30 μg/L SDF-1 to RPCs increased from 13.00％ in 16％ O2 culture group to 36.00％ and 46.00％ in the cells cultured by 10％ O2for 12 and 24 hours.FACS revealed that the proportion of CXCR4+ cells in hypoxia-exposure for 12 and 24 hours were 26.90％ and 46.10％,respectively,but that in 16％ O2 culture group was 9.10％,showing a statistically significant difference(P ＜ 0.01).Conclusions RPCs induced by hypoxia can enhance the expression of CXCR4 in RPE cells and the chemotaxia to SDF-1.The overexpression of H1F-1 in RPCs may be involved in the up-regulation of CXCR4 expression.