CAJ | 학술논문

背景糖尿病视网膜病变(DR)是糖尿病常见的眼部并发症,其发病机制与多种因素有关,c-jun N末端激酶(JNK)作为一种凋亡基因,在糖尿病的病理过程中发挥着重要作用,其研究已成为近些年的热点之一,而JNK3作为JNK的亚基因之一,在DR中的研究目前较少.目的定量检测JNK3在糖尿病小鼠视网膜中的表达,探讨JNK3在DR中的作用.方法选取SPF级6～8周龄C57BL/6雄性小鼠48只,适应性喂养1周后按照随机数字表法分为糖尿病组和正常对照组.30只糖尿病组小鼠用一次性腹腔内注射柠檬酸钠缓冲液溶解的质量分数1％链脲佐菌素(STZ)的方法诱导糖尿病模型,18只对照组小鼠腹腔内注射等容量柠檬酸钠缓冲液.分别于造模后2、4、8周摘除小鼠左眼眼球,提取视网膜组织,采用实时定量PCR法检测JNK3 mRNA在小鼠视网膜中表达的动态变化.结果造模后2、4、8周,糖尿病组小鼠血糖水平明显高于正常对照组,差异均有统计学意义(t=-5.675、-5.498、-5.347,P＜0.01).糖尿病组和正常对照组在造模后不同时间点小鼠视网膜中JNK3 mRNA相对表达量(A值)的差异均有统计学意义(F分组=102.345,P＜0.05;F时间 =131.679,P＜0.05);其中造模后4周和8周糖尿病组小鼠视网膜中JNK3 mRNA相对表达量分别为3.21±0.14和5.43±0.37,均明显高于正常对照组的2.54 ±0.42和2.26±0.67,差异均有统计学意义(t=4.073、23.399,P＜0.05);糖尿病组内比较可见,造模后8周小鼠视网膜中JNK3 mRNA相对表达量明显高于2周和4周值,差异均有统计学意义(t=10.756、16.857,P＜0.05).结论 JNK3在糖尿病小鼠视网膜中表达量上调,其早期表达量随时间延长而增加.JNK3可能参与早期DR的发生和发展.
배경 당뇨병시망막병변(DR)시당뇨병상견적안부병발증,기발병궤제여다충인소유관,c-jun N말단격매(JNK)작위일충조망기인,재당뇨병적병리과정중발휘착중요작용,기연구이성위근사년적열점지일,이JNK3작위JNK적아기인지일,재DR중적연구목전교소.목적 정량검측JNK3재당뇨병소서시망막중적표체,탐토JNK3재DR중적작용.방법 선취SPF급6～8주령C57BL/6웅성소서48지,괄응성위양1주후안조수궤수자표법분위당뇨병조화정상대조조.30지당뇨병조소서용일차성복강내주사저몽산납완충액용해적질량분수1％련뇨좌균소(STZ)적방법유도당뇨병모형,18지대조조소서복강내주사등용량저몽산납완충액.분별우조모후2、4、8주적제소서좌안안구,제취시망막조직,채용실시정량PCR법검측JNK3 mRNA재소서시망막중표체적동태변화.결과 조모후2、4、8주,당뇨병조소서혈당수평명현고우정상대조조,차이균유통계학의의(t=-5.675、-5.498、-5.347,P＜0.01).당뇨병조화정상대조조재조모후불동시간점소서시망막중JNK3 mRNA상대표체량(A치)적차이균유통계학의의(F분조=102.345,P＜0.05;F시간 =131.679,P＜0.05);기중조모후4주화8주당뇨병조소서시망막중JNK3 mRNA상대표체량분별위3.21±0.14화5.43±0.37,균명현고우정상대조조적2.54 ±0.42화2.26±0.67,차이균유통계학의의(t=4.073、23.399,P＜0.05);당뇨병조내비교가견,조모후8주소서시망막중JNK3 mRNA상대표체량명현고우2주화4주치,차이균유통계학의의(t=10.756、16.857,P＜0.05).결론 JNK3재당뇨병소서시망막중표체량상조,기조기표체량수시간연장이증가.JNK3가능삼여조기DR적발생화발전.
Background Diabetic retinopathy (DR) is a common ocular complication of diabetes,and its pathogenesis is associated with a variety of factors.c-Jun N terminal kinase (JNK),one of the genes involving in apoptosis,plays an important role in the pathology of diabetes,and relative research is catching increasing interests in recent years.Objective This study was to quantify the expression of JNK3 in retinas of DR murine.Methods Forty-eight SPF male C57BL/6 mice were randomly divided into the diabetes group and the normal control group.Diabetic mouse models were establishend by intraperitoneal injection of 1％ streptozocin (STZ) dissolved by sodium citrate buffer,and equvilant volume of sodium citrate buffer was used in the same way in the mice of the control mice.The left eyeballs were obtained 2,4,8 weeks after modeling and the retinas were collected.Real-time quantitaive PCR was perfored to detect the expression of JNK3 mRNA in retinas.The use and care of the experimental mice complied with the Administration of Experimental Animals in Kunming Medical College.Results Blood glucose levels were significantly higher in 2,4,8 weeks after modeling in the diabetic group compared with the normal control group (t=-5.675,-5.498,-5.347,all at P＜0.01).The relative expression levels of JNK3 mRNA (A value) in the retinas were significantly different between the groups at various time points (Fgroup =102.345,P＜0.05 ; Ftime =131.679,P＜ 0.05).The relative expression levels of JNK3 mRNA in the retinas were 3.21 ±0.14 and 5.43 ±O.37 in 4 and 8 weeks after modeling in the diabetic group,which were significantly elevated in comparison with the normal control group (2.54±0.42 versus 2.26±0.67) (t =4.073,23.399,both at P＜0.05).Compared with the second week and fourth week,the relative expression levels of JNK3 mRNA in the retinas in the eighth week were significantly raised in the diabetic group (t =10.756,16.857,both at P ＜ 0.05).Conclusions JNK3 expression in the retina upregulates in diabtic mice in a time-dependent manner.JNK3 is paopably involved in the pathogenesis and development of DR.