糖皮质激素诱发白内障与Ca^(2+)介导效应的实验研究

Effects of calcium on glucocorticoid-induced cataract in chicken embryo

目的研究钙(Ca2+)在糖皮质激素诱发晶状体代谢紊乱过程中的介导作用。方法应用免疫印迹技术探查鸡胚肝脏和晶状体组织中糖皮质激素特异性受体的表达;应用原子吸收光谱分析技术对Ca2+通道阻滞剂维拉帕米对钙在诱发过程中的介导作用进行分析。结果免疫印迹分析结果显示鸡胚肝脏组织中有糖皮质激素受体(93000)表达,而晶状体组织中则未有显示;维拉帕米可以抑制糖皮质激素作用条件下晶状体内Ca2+浓度的累聚、降低晶状体的混浊程度。结论糖皮质激素通过间接的、非特异性受体途径诱发晶状体代谢的紊乱,Ca2+具有重要的介导作用。

Objective To investigate the relationship between glucocorticoid-induced cataract and calcium-mediated effect and the role of verapamil,a calcium channel blocker,on this process. Methods Eighty 15-day-old chicken embryos were divided into control group ( n = 25 ) , glucocorticoid group (n = 25 , dexamethasone 0. 025 μmol/per egg) and glucocorticoid + verapamil group (n = 30,dexamethasone 0. 025 μmol + Verapamil 0. 5 mg /per egg). All lenses were extracted after 24 hours. The opacity of lenses were inspected under slit lamp microscope and photographed by digital camera under the same illumination condition. Western blotting with a specific glucocorticoid receptor antibody was used to determine the expression of glucocortoid receptor in lenses. Lenticular calcium, magnesium and iron levels were measured with an atomic spectrophotometer. Results Western blotting with a specific glucocorticoid receptor antibody revealed protein bands of approximately 93 000 in liver,showing a positive expression of glucocortoid receptor in liver of chicken embryo, but no immunoreactivity was observed in lenses. Microscopic inspection of the lenses determined posterior subcapsular opacity in both the glucocorticoid group and glucocortoid + verapamil group,but the former was more severe (P < 0. 01). Calcium level in the glucocorticoid group was significantly higher than that in the glucocortoid + verapamil group (P < 0. 01). Verapamil significantly reduced the lenticular content of calcium, magnesium and iron. Conclusion Imbalance of lens calcium may be one of the key factors in glucocorticoid cataract genesis. As a calcium channel blocker, Verapamil can decrease the risk of glucocorticoid-induced cataract.