CAJ | 학술논문

目的在高盐饮食诱导盐敏感大鼠高血压模型中,研究肾脏内源性硫化氢(H2S)体系的变化规律.方法 16只雄性Dah1大鼠采用随机数字表法分为对照组和高盐组(饲料中盐质量分数为80g/kg),每组8只.实验8周后,测定24 h尿钠、24h尿蛋白、血清肌酐和血清尿素,观察肾脏显微和超微结构改变,敏感硫电极法测定血清和肾组织H2S水平,实时荧光定量聚合酶链反应(RT-PCR)检测肾组织内源性H2S生成关键酶胱硫醚β-合酶(CBS)、胱硫醚γ-裂解酶(CSE)和巯基丙酮酸硫基转移酶(MPST) mRNA表达,Western blot检测肾组织CBS、CSE和MPST蛋白表达.结果与对照组比较,高盐组Dah1大鼠血压显著升高,肾功能下降,肾脏病变明显,表现为肾小球节段型硬化,肾小动脉管壁增厚,管腔闭塞.高盐组Dah1大鼠肾脏内源性H2S体系显著下调,表现为血清和肾组织H2S水平下降,肾组织CBS、CSE和MPST mRNA表达降低,CBS蛋白表达降低.结论高盐饮食刺激Dah1大鼠形成高血压及肾脏损害,肾脏内源性H2S/CBS体系下调.
목적 재고염음식유도염민감대서고혈압모형중,연구신장내원성류화경(H2S)체계적변화규률.방법 16지웅성Dah1대서채용수궤수자표법분위대조조화고염조(사료중염질량분수위80g/kg),매조8지.실험8주후,측정24 h뇨납、24h뇨단백、혈청기항화혈청뇨소,관찰신장현미화초미결구개변,민감류전겁법측정혈청화신조직H2S수평,실시형광정량취합매련반응(RT-PCR)검측신조직내원성H2S생성관건매광류미β-합매(CBS)、광류미γ-렬해매(CSE)화구기병동산류기전이매(MPST) mRNA표체,Western blot검측신조직CBS、CSE화MPST단백표체.결과 여대조조비교,고염조Dah1대서혈압현저승고,신공능하강,신장병변명현,표현위신소구절단형경화,신소동맥관벽증후,관강폐새.고염조Dah1대서신장내원성H2S체계현저하조,표현위혈청화신조직H2S수평하강,신조직CBS、CSE화MPST mRNA표체강저,CBS단백표체강저.결론 고염음식자격Dah1대서형성고혈압급신장손해,신장내원성H2S/CBS체계하조.
Objective To study the change of the renal endogenous hydrogen sulfide (H2 S) pathway in the development of salt-sensitive hypertension in Dah1 rats.Methods Sixteen male Dah1 rats,in accordance with the random number table,were randomly divided into control group and high salt group fed with diet containing 80 g/kg NaCl.After 8 weeks,24 h urine sodium,24 h urinary protein,serum creatinine and serum urea were measured.The microstructural and ultrastructural changes in kidney were observed with light microscope and electronic microscope.The serum and kidney H2S contents were determined by using sulphur-sensitive electrode method.The mRNA levels of cystathionine β-synthase(CBS),cystathionine γ-lyase(CSE) and mercaptopyruvate sulfurtransferase(MPST) in renal tissue were determined by means of real-time polymerase chain reaction(RT-PCR).The protein expressions of CBS,CSE and MPST in renal tissue were detected by using Western blot.Results Compared with control group,high salt group rats had a significant rise in blood pressure,declined renal function,damaged renal structure,segmental glomerular sclero sis,small artery wall thickening,and occlusion of the lumen.Moreover,the endogenous H2S pathway in kidney of Dah1rats with high salt diet was downregulated markedly,demonstrated by the decreased serum and kidney H2S content,the reduced renal CBS,CSE and MPST mRNA expressions and CBS protein expression of kidney tissue.Conclusion The endogenous H2S/CBS pathway is downregulated during the development of salt-sensitive hypertension in Dah1 rats.