CAJ | 학술논문

背景糖尿病视网膜病变(DR)的分子生物学发病机制仍不清楚,以往的研究表明内质网应激相关因子在糖尿病患者外周血中呈高表达,而P58 IPK 可以抑制这些因子的表达,因此P58 IPK 和糖尿病之间的关系值得深入研究.目的检测P58 IPK 在糖尿病大鼠模型视网膜中的动态表达,为进一步研究P58 IPK 抑制DR的机制奠定基础.方法 18只SD大鼠腹腔注射60 mg/kg链脲佐菌素(STZ)制作糖尿病动物模型,分别于造模后1、3、6个月各处死6只大鼠;另6只匹配的正常SD大鼠作为正常对照组.取视网膜组织采用实时定量聚合酶链反应(real-time PCR)法检测P58 IPK mRNA在大鼠视网膜中的表达,观察P58 IPK mRNA随糖尿病的发展出现的动态变化.结果造模后糖尿病组大鼠表现出多饮、多食、多尿,血糖均≥16.5 mmol/L,造模成功率为100%.造模后1个月、3个月鼠视网膜中P58 IPK mRNA/β-actinm RNA 的A值分别为0.800±0.005和0.975±0.008,明显高于对照组的0.725±0.006,差异有统计学意义(t=22.589、t=62.784,P＜0.05),造模后6个月鼠视网膜P58 IPK/β-actin的A值为0.671±0.004,并明显低于对照组,差异有统计学意义(t=-17.984,P＜0.05).结论 P58 IPK 参与DR的发病机制,可能具有延缓DR发生和发展的作用.
배경당뇨병시망막병변(DR)적분자생물학발병궤제잉불청초,이왕적연구표명내질망응격상관인자재당뇨병환자외주혈중정고표체,이P58 IPK 가이억제저사인자적표체,인차P58 IPK 화당뇨병지간적관계치득심입연구.목적검측P58 IPK 재당뇨병대서모형시망막중적동태표체,위진일보연구P58 IPK 억제DR적궤제전정기출.방법 18지SD대서복강주사60 mg/kg련뇨좌균소(STZ)제작당뇨병동물모형,분별우조모후1、3、6개월각처사6지대서;령6지필배적정상SD대서작위정상대조조.취시망막조직채용실시정량취합매련반응(real-time PCR)법검측P58 IPK mRNA재대서시망막중적표체,관찰P58 IPK mRNA수당뇨병적발전출현적동태변화.결과조모후당뇨병조대서표현출다음、다식、다뇨,혈당균≥16.5 mmol/L,조모성공솔위100%.조모후1개월、3개월서시망막중P58 IPK mRNA/β-actinm RNA 적A치분별위0.800±0.005화0.975±0.008,명현고우대조조적0.725±0.006,차이유통계학의의(t=22.589、t=62.784,P＜0.05),조모후6개월서시망막P58 IPK/β-actin적A치위0.671±0.004,병명현저우대조조,차이유통계학의의(t=-17.984,P＜0.05).결론 P58 IPK 삼여DR적발병궤제,가능구유연완DR발생화발전적작용.
Background The molecular biological mechanisms of diabetic retinopathy(DR)is unclear up to now.Researches have proved that endoplasmic reticulum stress(ER Stress)-associated factors are elevated in peripheral blood in patients with diabetic retinopathy.and P58 IPK can inhibit those factors.So the relationship between P58 IPK and DR is worth to investigate. Objective The aim of this study was to detect the dynamic expression of P58 IPK in the retina of diabetic rats. Methods The diabetic animal models were established in 18 clean male SD rats by intraperitoneal injection of stilptozotiein(STZ)at a dose of 60 mg/kg.The rats were sacrificed in 1,3,6 months after injection.The expression change of P58 IPK mRNA in the rats retina was detected by quantitative real-time RT-PCR.Other 6 matched normal rats were used as control groups.This experiment followed the Regulations for the Administration of Affair Concerning experimental Animals by State Science and Technology Commission. Results The rats showed more drinking,more food and more urine after STZ injection with the blood glucose level≥ 16.5 mmol/L.The success rate of diabetic models was 100%.The A value of P58 IPK mRNA/β-actin in rat retina was 0.800±0.005 and 0.975±0.008 after injection of STZ.and that of control rats was 0.725±0.006,showing statistically significant difference between them(t=22.589,t=62.784,P＜0.05).In 6 months after injection of STZ,the expression of P58 IPK mRNA in experimental diabetic rat retina was evidently lower than the eontrol rats(0.671±0.004 versus 0.725±0.006,t=-17.984,P＜0.05).Conclusion P58 IPK has a close relation to the pathogenesis of DR,and it plays a retarding role for DR.