ABSTRACT
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.
ABSTRACT
BACKGROUND: Vitamin D3 up-regulated protein 1 (VDUP1) gene is known to be a novel member of the early response genes and an oxidative stress mediator. This study was designed to elucidate VDUP1 expression and its involvement in central sensitization after spinal cord injury (SCI). METHODS: Contusion injury was produced at spinal segment T10 (20 mm drop, 10 g rod) in adult male Sprague-Dawley rats (250 300 g). Withdrawal responses were measured using von Frey filaments and acetone on the 1st, 3rd and 7th days after SCI. The expressions of VDUP1 gene in the brain and in the cervical and lumbar spine were examined by immunohistochemistry on the 1st, 3rd and 7th day after SCI. RESULTS: VDUP1 gene was detected in a few oligodendrocytes in the spinal cord and in the brain of control rats. VDUP1 gene expression increased in most of the neurons and ependymal cells in the central canal of the injured (lumbar) spinal cord 1 day after SCI. This expression gradually decreased in majority of cells from day 1 to day 7 after SCI. VDUP1 gene expression was also observed to be increased 1 day after SCI, and gradually to decrease from 1 day to 7 days after SCI. The neurons in the intact (cervical) spinal cord VDUP1 gene expression increases maximally 3 days after SCI in the cerebral cortex and the thalamus. Neuropathic pain behavior was triggered by the plantar surface of the fore foot after SCI. CONCLUSIONS: These results show that the VDUP1 gene may be an early modulator of transneuronal stress response after SCI, and to be related to the central sensitization of neuropathic pain behavior after SCI.