CAJ | 학술논문

目的观察链脲佐菌素(STZ)诱导的糖尿病大鼠在不同时期其血清脂联素和脂联素受体(AdipoR)在肾脏组织的表达水平.方法 64只雌性SD大鼠按随机数字表法分为对照组和实验组(分别为2、6、10、12周,共8组):实验组大鼠32只,一次性空腹腹腔注射STZ 60 mg/kg,诱导糖尿病大鼠模型;对照组大鼠32只,腹腔注射等体积的枸橼酸缓冲液.分别于糖尿病大鼠成模后第2、6、10、12周两组各取8只,测体重、肾重、空腹血糖、24 h尿白蛋白定量;心内采血,离心取血清,检测血肌酐,空腹血清胰岛素;ELISA方法检测血、尿脂联素浓度.取左肾常规病理组织行糖原染色,在光镜下观察肾脏的病理组织学改变,免疫组化SP法检测肾脏2种受体AdipoR1和AdipoR2表达.结果 (1)实验组6、10、12周大鼠血清和尿脂联素高于对照组,差异有统计学意义(P＜0.01);且血清脂联素与24 h尿白蛋白排泄率、尿脂联素呈正相关(r值分别为0.806、0.696,均P＜0.01);尿脂联素与24 h尿白蛋白定量呈显著正相关(r=0.728,P＜0.01);逐步回归分析提示血清脂联素受24 h尿白蛋白定量影响最大(β=0.806,P＜0.01);(2)免疫组化半定量分析显示,AdipoR1和AdipoR2在正常大鼠肾组织中均有表达,主要分布于肾小管上皮细胞和肾小球内皮细胞.实验组造模成功6周时肾脏组织AdipoR1和AdipoR2表达,与对照组比较表达有所增强(F值分别为11.68、23.20,均P＜0.01),且与血清脂联素呈显著正相关(r值分别为0.666、0.684,均P＜0.01).结论血清和尿脂联素水平与糖尿病肾病病程和AdipoR呈正相关,推测脂联素通过AdipoR直接作用于肾脏,尤其是作用于肾小管,在1型糖尿病肾脏病变中发挥保护作用.
목적 관찰련뇨좌균소(STZ)유도적당뇨병대서재불동시기기혈청지련소화지련소수체(AdipoR)재신장조직적표체수평.방법 64지자성SD대서안수궤수자표법분위대조조화실험조(분별위2、6、10、12주,공8조):실험조대서32지,일차성공복복강주사STZ 60 mg/kg,유도당뇨병대서모형;대조조대서32지,복강주사등체적적구연산완충액.분별우당뇨병대서성모후제2、6、10、12주량조각취8지,측체중、신중、공복혈당、24 h뇨백단백정량;심내채혈,리심취혈청,검측혈기항,공복혈청이도소;ELISA방법검측혈、뇨지련소농도.취좌신상규병리조직행당원염색,재광경하관찰신장적병리조직학개변,면역조화SP법검측신장2충수체AdipoR1화AdipoR2표체.결과 (1)실험조6、10、12주대서혈청화뇨지련소고우대조조,차이유통계학의의(P＜0.01);차혈청지련소여24 h뇨백단백배설솔、뇨지련소정정상관(r치분별위0.806、0.696,균P＜0.01);뇨지련소여24 h뇨백단백정량정현저정상관(r=0.728,P＜0.01);축보회귀분석제시혈청지련소수24 h뇨백단백정량영향최대(β=0.806,P＜0.01);(2)면역조화반정량분석현시,AdipoR1화AdipoR2재정상대서신조직중균유표체,주요분포우신소관상피세포화신소구내피세포.실험조조모성공6주시신장조직AdipoR1화AdipoR2표체,여대조조비교표체유소증강(F치분별위11.68、23.20,균P＜0.01),차여혈청지련소정현저정상관(r치분별위0.666、0.684,균P＜0.01).결론 혈청화뇨지련소수평여당뇨병신병병정화AdipoR정정상관,추측지련소통과AdipoR직접작용우신장,우기시작용우신소관,재1형당뇨병신장병변중발휘보호작용.
Objective To explore the role of adiponectin and receptors of adiponectin ( AdipoR1,AdipoR2) in the development of diabetic kidney disease (DKD) in diabetes mellitus rats induced by streptozotocin (STZ). Methods A total of 64 SD rats were randomly divided into two groups. Thirty-two rats were in normal control(NC) group and the others were in diabetes mellitus(DM) group. The rats in DM group were injected STZ intraperitoneally with a dose of 60 mg/kg while the ones in NC group were only done with the same dose of citric acid buffer. At 2,6,10 and 12 weeks, weight,fast blood glucose and 24-hour urinary albumin excretion were recorded, serum fast blood insulin was also measured. Adiponectin levels in urine and serum were evaluated by ELISA. The pathological changes of kidney were examined by light microscope. Renal expression of AdipoR1, AdipoR2 was determined by immunohistochemistry. Results ( 1 ) The levels of adiponectin in urine and blood in DM group were higher than that in NC group after 2 weeks(6 weeks, 10 weeks, 12 weeks, P ＜0. 01 ) and increased gradually during the whole experiment.Correlative analyses revealed a positive correlation between serum adiponectin and the quantification of albumin in 24 h urine, urinary adiponectin ( r = 0. 806, P ＜ 0. 01; r = 0. 696, P ＜ 0.01 ) and between urinary adiponectin and the quantification of albumin in 24 h urine ( r = 0. 728, P ＜ 0.01 ). Stepwise regression analyses showed that the quantification of albumin in 24 h urine was independently associated with adiponectin concentrations( β =0. 806, P ＜0.01 ). (2) Compared the NC group,the expressions of AdipoR1 and AdipoR2 in kidney tissue were enhanced in DM group, and increased gradually (F value was 11.68,23. 20,respectively). There was a significant positive correlation between adiponectin and AdipoR1 and AdipoR2 in DM group(r =0.666, P＜0.001; r=0.684, P＜0.01). Conclusion With the progression of DM, the levers of adiponectin and its receptors increase which shows a significant protective effect in renal damage.