CAJ | 학술논문

目的观察糖尿病大鼠膀胱中肾上腺素能β3受体(β3-AR)的表达在糖尿病膀胱病变发生发展中的作用.方法将80只大鼠按随机化原则分为糖尿病模型组(n=40)及正常对照组(n=40).应用链脲佐菌素60 mg/kg腹腔注射,诱导形成Ⅰ型糖尿病大鼠模型,分别在发病第2、4、6、8、10周时处死取全膀胱,称重,取材制作光镜病理标本及提取蛋白,采用蛋白印迹法检测各组大鼠膀胱逼尿肌细胞肾上腺素能β3受体蛋白的表达.结果糖尿病模型组大鼠体质量组增长缓慢,膀胱湿重增加(P＜0.05).糖尿病组膀胱逼尿肌细胞肥大,变性,排列紊乱松散,胶原及纤维组织明显增生,出现空泡；晚期逼尿肌细胞萎缩,仅见大量的胶原及弹性纤维成分.糖尿病大鼠膀胱逼尿肌细胞肾上腺素能β3受体蛋白表达高于正常对照组(P＜0.05)；2周:(0.73±0.09)比(0.35±0.04),4周:(0.81±0.13)比(0.32±0.06),6周:(0.72±0.05)比(0.33±0.04),8周:(0.55±0.07)比(0.33 ±0.06),10周:(0.52±0.07)比(0.33±0.05)(P＜0.05).结论各时间段的糖尿病组膀胱逼尿肌均出现损害,各时间段的糖尿病组膀胱逼尿肌细胞中肾上腺素能β3受体含量均增加,肾上腺素能β3受体在糖尿病膀胱病变的发生发展中发挥重要作用.
목적 관찰당뇨병대서방광중신상선소능β3수체(β3-AR)적표체재당뇨병방광병변발생발전중적작용.방법 장80지대서안수궤화원칙분위당뇨병모형조(n=40)급정상대조조(n=40).응용련뇨좌균소60 mg/kg복강주사,유도형성Ⅰ형당뇨병대서모형,분별재발병제2、4、6、8、10주시처사취전방광,칭중,취재제작광경병리표본급제취단백,채용단백인적법검측각조대서방광핍뇨기세포신상선소능β3수체단백적표체.결과 당뇨병모형조대서체질량조증장완만,방광습중증가(P＜0.05).당뇨병조방광핍뇨기세포비대,변성,배렬문란송산,효원급섬유조직명현증생,출현공포；만기핍뇨기세포위축,부견대량적효원급탄성섬유성분.당뇨병대서방광핍뇨기세포신상선소능β3수체단백표체고우정상대조조(P＜0.05)；2주:(0.73±0.09)비(0.35±0.04),4주:(0.81±0.13)비(0.32±0.06),6주:(0.72±0.05)비(0.33±0.04),8주:(0.55±0.07)비(0.33 ±0.06),10주:(0.52±0.07)비(0.33±0.05)(P＜0.05).결론 각시간단적당뇨병조방광핍뇨기균출현손해,각시간단적당뇨병조방광핍뇨기세포중신상선소능β3수체함량균증가,신상선소능β3수체재당뇨병방광병변적발생발전중발휘중요작용.
Objective To investigate the expression of β3-adrenergic receptor (β3-AR) and detrusor injury in the bladder of rats with diabetic mellitus.Methods Eighty female Wistar rats were randomly divided into the diabetic model group ( n =40) and the normal control group ( n =40).The rat type 1 diabetes mellitus model was induced by peritoneal injection of the streptozotocin.The experiments were carried out at corresponding time points after the nodel was successfully set up,and the blood glucose (BG) levels were measured to exclude those rats with BG ≤ 16.7 mmol/L.The bladders were completely cut down and the bladder wet weight was measured.After hematoxylin and eosin (HE) staining,the morphological changes of the bladder detrusor in diabetic rats were observed under the light microscope.The expression of β3-AR protein was detected by using Western blotting.Results Routine pathologic examinations of the bladder detrusor smooth muscle:Under the light microscope,detrusor structure in every group was observed.In diabetic model group,transitional epithelium cell arrangement was not intact.Membrana propria was hyperemia and dropsy and size of decompensated detrusor muscle cell was large and the degeneration appeared,the shape was diverse and interstitial collagen component increased.After that,Muscle fiber was arranged disorder and out of order,cross of muscle fiber was full and space between the muscle fiber was enlarged obviously.The collagen and fiber structure was obviously proliferated and a lot of collagen could be seen.Finally detrusor cell atrophied,reduced or even disappeared,and only a lot of collagen and elastic fiber components could be seen.The change in β3-AR protein of the bladder detrusor smooth muscle:The result of Western blotting demonstrated that the amount of β3-AR protein in diabetic rat bladder was increased than control bladder [2 w:(0.73 ±0.09) vs (0.35 ±0.04),4 w:(0.81 ±0.13) vs (0.32 ±0.06),6 w:(0.72 ±0.05) vs (0.33 ±0.04),8 w:(0.55 ±0.07) vs (0.33 ±0.06),10 w:(0.52 ±0.07) vs (0.33 ±0.05) (P ＜0.05) ],what' s more important,the amount of β3-AR protein in 2-week-diabetic model group,4-week-diabetic model group and 6-wee-k-diabetic model group increased more obvious.Conclusion The bladder detrusor smooth muscle of every diabetic model rats group was injured.The expressed levels of β3-adrenergic receptor were increased in the bladder detrusor smooth muscle of every diabetic model rats group with streptozotocin injection.The expressed change of β3-adrenergic receptor played an important role in the development of diabetic cystopathy (DCP).