CAJ | 학술논문

背景:糖尿病视网膜病变是糖尿病普通的并发症,牛磺酸是视网膜中含量最丰富的游离氨基酸,它是视网膜再生和发育必需的营养因子,缺乏牛磺酸会引起视网膜结构和功能改变. 目的:探讨牛磺酸对糖尿病大鼠视网膜神经胶质原纤维酸性蛋白mR-NA及其蛋白表达的影响.设计:随机对照观察.单位:中国人民解放军第三军医大学.材料:试验于2003-3/2003-12在第三军医大学完成.选取封闭群SD大鼠54只,体质量为250 g.将造模成功的糖尿病大鼠54只随机分为糖尿病1月组、牛磺酸干预糖尿病1月组、糖尿病2月组、牛磺酸干预糖尿病2月组、糖尿病3月组和牛磺酸干预糖尿病3月组6组,每组9只.同期选取正常对照组共15只.方法:动物单笼喂养,自由进食饮水,实验前禁食12 h,用链脲佐菌素诱导糖尿病,用尿糖试纸测尿糖达(+++)以上,尾静脉采血测血糖浓度大于16.7 mmol/L即为模型建立成功.采用免疫组化、RT-PCR和Western blotting等技术方法,检测神经胶质原纤维酸性蛋白mRNA和蛋白的表达.观察牛磺酸对糖尿病视网膜病变大鼠神经元及神经胶质细胞的影响.主要观察指标:观察神经胶质原纤维酸性蛋白mRNA和蛋白表达.结果:①免疫组化分析显示:糖尿病大鼠1个月时,牛磺酸即可抑制神经胶质原纤维酸性蛋白的免疫反应性,随着牛磺酸干预时间的延长,神经胶质原纤维酸性蛋白免疫反应性渐弱.②RT-PCR检测:2个月始,糖尿病组神经胶质原纤维酸性蛋白mRNA的表达开始增大,牛磺酸明显下调神经胶质原纤维酸性蛋白mRNA的表达.③3个月的糖尿病组神经胶质原纤维酸性蛋白蛋白表达最强.牛磺酸干预糖尿病大鼠2个月时,神经胶质原纤维酸性蛋白表达减少.结论:牛磺酸可下调神经胶质原纤维酸性蛋白及mRNA表达,对糖尿病视网膜病变具有保护作用.
배경:당뇨병시망막병변시당뇨병보통적병발증,우광산시시망막중함량최봉부적유리안기산,타시시망막재생화발육필수적영양인자,결핍우광산회인기시망막결구화공능개변. 목적:탐토우광산대당뇨병대서시망막신경효질원섬유산성단백mR-NA급기단백표체적영향.설계:수궤대조관찰.단위:중국인민해방군제삼군의대학.재료:시험우2003-3/2003-12재제삼군의대학완성.선취봉폐군SD대서54지,체질량위250 g.장조모성공적당뇨병대서54지수궤분위당뇨병1월조、우광산간예당뇨병1월조、당뇨병2월조、우광산간예당뇨병2월조、당뇨병3월조화우광산간예당뇨병3월조6조,매조9지.동기선취정상대조조공15지.방법:동물단롱위양,자유진식음수,실험전금식12 h,용련뇨좌균소유도당뇨병,용뇨당시지측뇨당체(+++)이상,미정맥채혈측혈당농도대우16.7 mmol/L즉위모형건립성공.채용면역조화、RT-PCR화Western blotting등기술방법,검측신경효질원섬유산성단백mRNA화단백적표체.관찰우광산대당뇨병시망막병변대서신경원급신경효질세포적영향.주요관찰지표:관찰신경효질원섬유산성단백mRNA화단백표체.결과:①면역조화분석현시:당뇨병대서1개월시,우광산즉가억제신경효질원섬유산성단백적면역반응성,수착우광산간예시간적연장,신경효질원섬유산성단백면역반응성점약.②RT-PCR검측:2개월시,당뇨병조신경효질원섬유산성단백mRNA적표체개시증대,우광산명현하조신경효질원섬유산성단백mRNA적표체.③3개월적당뇨병조신경효질원섬유산성단백단백표체최강.우광산간예당뇨병대서2개월시,신경효질원섬유산성단백표체감소.결론:우광산가하조신경효질원섬유산성단백급mRNA표체,대당뇨병시망막병변구유보호작용.
BACKGROUND: Diabetic retinopathy is the common complications of diabetes mellitus. Taurine is free aminoacid with the mostly abundant content in retina, and it is the necessary nutrition factor for regeneration and development of retina. Deficiency of taurine will cause structural and functional change of retina.OBJECTIVE: To probe into the effect of taurine on the expression of retinal glial fibrillary acidic protein (GFAP) mRNA DESIGN: A randomized and controlled observation SETTING: Third Military Medical University of Chinese PLA MATERIALS: This experiment was carried out at the Third Military Medical University of Chinese PLA from March 2003 to December 2003.Totally 54 closed group SD rats, with body mass of 250 g, were chosen.The successful diabetic rat model were randomly divided into 6 groups: diabetic group of 1 month, taurine-treated diabetic group of 1 month, diabetic group of 2 months, taurine-treated diabetic group of 2 months, diabetic group of 3 months, taurine-treated diabetic group of 3 months, with 9 rats in each group. Another 15 rats were chosen homeochronously as normal control group.METHODS: The animals were raised in separate cages. They were free to access to food and water, and fasted for 12 hours before experiment. Streptozotocin was used to induce diabetes mellitus .When Tes-Tape showed urine glucose reached more than (+++), and blood glucose concentration of venous blood from tail measured ＞16.7 mmol/L, models were established successfully. Expressions of GFAP mRNA and protein were measured with immunohistochemistry, RT-PCR, Western blotting and other technical methods. The effect of taurine on retinal neurons and glial cells in rats with diabetes mellitus was observed.MAIN OUTCOME MEASURES: Expressions of GFAP mRNA and protein RESULTS: ① Immunohistochemical analysis showed that: When rats suffered from diabetes mellitus for 1 month, taurine can inhibit the immunoreactivity of GFAP. With the elongation of intervention time of taurine, the immunoreactivity of GFAP is weakened. ②RT-PCR detection: Starting from the beginning of 2 months, the expression of GFAPmRNA in diabetic group began to increase; taurine obviously down-regulated the expression of GFAP mRNA. ③ In taurine-treated diabetic group of 3 months,the expression of GFAP was the strongest. When diabetic rats were treated by taurine for 2 months, the expression of GFAP was decreased.CONCLUSION: Taurine can down-regulate the expression of GFAP mR-NA and protein, indicating that it can protect retinal pathological change in rats with diabetes mellitus.