中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
CHINESE JOURNAL OF EXPERIMENTAL SURGERY
2013年
6期
1126-1128
,共3页
郑湘予%王焱%朱志强%文建国
鄭湘予%王焱%硃誌彊%文建國
정상여%왕염%주지강%문건국
输尿管梗阻%水通道蛋白2%替米沙坦%肾功能
輸尿管梗阻%水通道蛋白2%替米沙坦%腎功能
수뇨관경조%수통도단백2%체미사탄%신공능
Ureteral obstruction%Aquaporin 2%Telmisartan%Renal function
目的 观察替米沙坦对双侧输尿管梗阻(BUO)大鼠水电解质紊乱和肾脏水通道蛋白2(AQP2)表达的影响.方法 慕尼黑大鼠36只,随机分为BUO组、替米沙坦组(TEL组)和对照组(Sham组),每组12只.BUO组和TEL组均行双侧输尿管结扎术,Sham组仅游离输尿管但不结扎.TEL组每天TEL液灌胃[5 mg/(kg·d)],BUO组和Sham组同体积生理盐水灌胃.双侧输尿管梗阻24 h后解除梗阻,第4天收集血液和肾脏标本,采用免疫组织化学和Western blot技术检测肾脏AQP2表达.结果 BUO组与Sham组比较,尿量显著增高[(93 6) μl/(min· kg)比(26 ±4)μl/(min· kg)],尿比重和尿钠显著降低[1.007±0.007比1.024±0.017；(43.25±6.99) mmol/L比(182.37±17.91) mmoL/L],血肌酐和血清钾显著增高[(66.22±6.03) μmol/L比(33.89 2.97)μmol/L; (5.57 0.37) mmol/L比(4.29±0.09) mmol/L].TEL组与BUO组比较,尿量显著降低(54 6) μl/(min·kg)比(93 6) μ1/(min· kg),尿比重和尿钠显著升高[1.017 0.009比1.007±0.007；(82.23±12.98) mmol/L比(43.25±6.99) mmol/L],血肌酐和血清钾显著降低[(42.83±1.51) μmol/L比(66.22 ±6.03) μmol/L; (4.69±0.21) mmol/L比(5.57±0.37) mmol/L].AQP2表达BUO组显著低于Sham组,TEL组显著高于BUO组,各组比较差异有统计学意义(P＜0.05).结论 替米沙坦可抑制AQP2蛋白表达下调,减轻BUO解除后肾脏低渗性尿,保护肾脏功能.
目的 觀察替米沙坦對雙側輸尿管梗阻(BUO)大鼠水電解質紊亂和腎髒水通道蛋白2(AQP2)錶達的影響.方法 慕尼黑大鼠36隻,隨機分為BUO組、替米沙坦組(TEL組)和對照組(Sham組),每組12隻.BUO組和TEL組均行雙側輸尿管結扎術,Sham組僅遊離輸尿管但不結扎.TEL組每天TEL液灌胃[5 mg/(kg·d)],BUO組和Sham組同體積生理鹽水灌胃.雙側輸尿管梗阻24 h後解除梗阻,第4天收集血液和腎髒標本,採用免疫組織化學和Western blot技術檢測腎髒AQP2錶達.結果 BUO組與Sham組比較,尿量顯著增高[(93 6) μl/(min· kg)比(26 ±4)μl/(min· kg)],尿比重和尿鈉顯著降低[1.007±0.007比1.024±0.017；(43.25±6.99) mmol/L比(182.37±17.91) mmoL/L],血肌酐和血清鉀顯著增高[(66.22±6.03) μmol/L比(33.89 2.97)μmol/L; (5.57 0.37) mmol/L比(4.29±0.09) mmol/L].TEL組與BUO組比較,尿量顯著降低(54 6) μl/(min·kg)比(93 6) μ1/(min· kg),尿比重和尿鈉顯著升高[1.017 0.009比1.007±0.007；(82.23±12.98) mmol/L比(43.25±6.99) mmol/L],血肌酐和血清鉀顯著降低[(42.83±1.51) μmol/L比(66.22 ±6.03) μmol/L; (4.69±0.21) mmol/L比(5.57±0.37) mmol/L].AQP2錶達BUO組顯著低于Sham組,TEL組顯著高于BUO組,各組比較差異有統計學意義(P＜0.05).結論 替米沙坦可抑製AQP2蛋白錶達下調,減輕BUO解除後腎髒低滲性尿,保護腎髒功能.
목적 관찰체미사탄대쌍측수뇨관경조(BUO)대서수전해질문란화신장수통도단백2(AQP2)표체적영향.방법 모니흑대서36지,수궤분위BUO조、체미사탄조(TEL조)화대조조(Sham조),매조12지.BUO조화TEL조균행쌍측수뇨관결찰술,Sham조부유리수뇨관단불결찰.TEL조매천TEL액관위[5 mg/(kg·d)],BUO조화Sham조동체적생리염수관위.쌍측수뇨관경조24 h후해제경조,제4천수집혈액화신장표본,채용면역조직화학화Western blot기술검측신장AQP2표체.결과 BUO조여Sham조비교,뇨량현저증고[(93 6) μl/(min· kg)비(26 ±4)μl/(min· kg)],뇨비중화뇨납현저강저[1.007±0.007비1.024±0.017；(43.25±6.99) mmol/L비(182.37±17.91) mmoL/L],혈기항화혈청갑현저증고[(66.22±6.03) μmol/L비(33.89 2.97)μmol/L; (5.57 0.37) mmol/L비(4.29±0.09) mmol/L].TEL조여BUO조비교,뇨량현저강저(54 6) μl/(min·kg)비(93 6) μ1/(min· kg),뇨비중화뇨납현저승고[1.017 0.009비1.007±0.007；(82.23±12.98) mmol/L비(43.25±6.99) mmol/L],혈기항화혈청갑현저강저[(42.83±1.51) μmol/L비(66.22 ±6.03) μmol/L; (4.69±0.21) mmol/L비(5.57±0.37) mmol/L].AQP2표체BUO조현저저우Sham조,TEL조현저고우BUO조,각조비교차이유통계학의의(P＜0.05).결론 체미사탄가억제AQP2단백표체하조,감경BUO해제후신장저삼성뇨,보호신장공능.
Objective To explore the molecular mechanism of renal function defects after bilateral ureteral obstruction (BUO) and investigate the effect of telmisartan (TEL) on the expression of renal aquaporin 2 following BUO in rats.Methods Thirty-six Munich-Wistar rats were randomly divided into three groups (BUO,n =12 ; TEL,n =12 ; Sham,n =12).The BUO model was built in BUO and TEL groups by bilateral ureteral ligation.Age-and time-matched sham-operated controls were prepared.The rats in TEL group were fed on TEL [5 mg/(kg·d)] every day.BUO was released 24 h after BUO,and at the 4th day the blood samples were collected and kidneys were harvested to examine the effects of TEL on the dysregulation of AQP2 by using semi quantitative immunoblottling and immunohistochemistry.Results BUO resulted in a marked polyuria [BUO vs.sham:(93 ±6) μL/(min·kg) vs.(26 ±4) μ/(min·kg),n =12;P＜0.05] and a reduced urine specific gravity [BUO vs.sham:1.007 ±0.007 vs.1.024 ±0.017,n =12;P ＜0.05] and urine Na [(43.25 6.99) mmol/L vs.(182.37 ± 17.91) mmol/L,n =12 ; P ＜ 0.05],an increased Scr [(66.22 ±6.03) μmol/L vs.(33.89 ±2.97) μmol/L,n =12;P ＜0.05] and serum potassium [(5.57 0.37) mmol/L vs.(4.29 ±0.09) mmol/L,n =12;P ＜0.05].Administration of TEL partly prevented this increase in postobstructive urine production [(54 ±6) vs.(93 ±6) μL/(min·kg),n =12;P ＜0.05],and decrease in urine specific gravity (1.017 ± 0.009 vs.1.007 ± 0.007,n =12 ; P ＜ 0.05).TheScr and serum potassium levels were lower significantly in TEL group than in BUO group [(42.83 1.51)μmol/Lvs.(66.22 6.03) μmol/L; (4.69 ±0.21) mmol/L vs.(5.57 ±0.37) mmol/L,n=12;P＜0.05].BUO resulted in a significantly decreased expression of AQP2 as compared with controls,and TEL prevented the reduction of AQP2 (P ＜ 0.05).Conclusion TEL prevents dysregulation of AQP2 in response to BUO,demonstrating a marked renoprotective effect of TEL treatment in conditions with urinary tract obstruction.
