摘要
目的观察高盐摄入及补钾对Dahl盐敏感大鼠血压、肾髓质转化生长因子-β1(TGF-β1)及纤维化水平的影响,探讨TGF-β1在盐敏感高血压形成及靶器官损害中的作用。方法 6周龄雄性Dahl盐敏感大鼠(n=24)及SS-13BN大鼠(n=24)各3组,分别给予含4g/kg NaCl(低盐组)、80g/kg NaCl(高盐组)及80g/kg NaCl+80g/kg KCl(高盐补钾组)饮食干预4周。于干预前后测量大鼠尾动脉压。采用RT-PCR和免疫组化法测定肾髓质TGF-β1的表达,并用Masson染色观察肾髓质区的纤维化。结果经4周干预,Dahl盐敏感大鼠高盐组血压较低盐组明显升高[(169.9±2.2)mmHg vs.(147.1±6.1)mmHg,P<0.01],高盐补钾组较高盐组血压明显下降[(123.6±3.8)mmHg vs.(169.9±2.2)mmHg,P<0.01]。SS-13BN大鼠高盐组较低盐组血压升高[(145.6±1.9)mmHg vs.(140.2±3.7)mmHg,P<0.05],高盐补钾组较高盐组血压下降[(125.2±2.8)mmHg vs.(145.6±1.9)mmHg,P<0.01]。Dahl盐敏感大鼠高盐组TGF-β1mRNA及蛋白表达量较低盐组明显升高(0.87±0.02 vs.0.67±0.04,P<0.01;0.136±0.002 vs.0.030±0.002,P<0.01),高盐补钾组TGF-β1mRNA及蛋白表达量较高盐组明显减少(0.55±0.04 vs.0.87±0.02,P<0.01;0.070±0.008 vs.0.136±0.002,P<0.01)。Dahl盐敏感大鼠肾小管区胶原沉积高盐组多于低盐组(0.075±0.002 vs.0.037±0.002,P<0.01),高盐补钾组则较高盐组减少(0.038±0.008 vs.0.075±0.002,P<0.01)。结论高盐可使Dahl盐敏感大鼠血压明显升高,肾髓质区TGF-β1表达明显增加及纤维化。补钾对高盐引起的血压升高及靶器官损害有保护作用。
Objective To investigate the effects of high sodium and supplementary potassium intake on blood pressure, transforming growth factor （TGF-β1） expression and fibrosis of renal medulla of Dahl salt-sensitive rats so as to explore the effects of TGF-β1 on the occurrence of salt-sensitive hypertension and target organ damage. Methods We divided 24 six-week-old male Dahl salt-sensitive rats and 24 SS-13BN rats randomly into low salt group, high salt group, and high salt plus high potassium group, which were given 4 g/kg NaC1, 80/kg NaC1 and 80 g/kg NaC1 ＋ 80 g/kg KC1 diets, respectively, for four weeks. Their tail blood pressure was measured before and after the diet intervention. TGF-β1 expression in renal medulla was assessed by reverse transcription-PCR and immunohistochemical staining; the development of fibrosis in renal medulla was observed through Masson staining. Results After 4 weeks＇ diet intervention, in Dahl salt-sensitive rats, blood pressure increased significantly in high salt group compared with that in low salt group E （169.9± 2.2）mmHg vs. （147.1±6.1）mmHg, P〈0.01], that of the high salt plus potassium group was evidently decreased compared with that of high salt group （123.6~ 3.8 mmHg vs. 169.9--＋2.2 mmHg, P〈0.01）. In SS-13BN rats, blood pressure increased in high salt group compared with that in low salt group E（145.6±1.9）mmHg vs. （140.2±3.7）mmHg, P%0.05]3 that of high salt plus potassium group was decreased compared with that of high salt group （125.2± 2.8） mmHg vs. （ 145.6 ± 1.9） mmHg, P〈 0.01]. The mRNA and protein expressions of TGF-I？I in renal medulla of high salt group increased significantly compared with those of low salt group among Dahl salt-sensitive rats （0.87±0.02 vs. O. 67~0.04, P〈0.01; 0. 136±0. 002 vs. 0. 030±0. 002, P〈0.01）, and that of high salt plus potassium group decreased significantly compared with that of high salt group （0.55±0.04 vs. 0.87±0.02, P〈0.01; 0.070±0.008 vs. 0.136±0.002, P^0.01）. In Dahl salt-sensitive rats, there was more collagen deposition in renal tubular area in high salt group than in low salt group （0. 075±0. 002 vs. 0. 037±0. 002, P^0.01）. and that of the high salt plus potassium group decreased significantly compared with that of high salt group （0. 038-＋0. 008 vs. O. 075---＋-_0. 002, P%0.01）. Conclusion High-salt diet can cause significant rise in blood pressure and TGF-t31 expression, and lead to fibrosis of renal medulla in Dahl salt- sensitive rats. Supplementation of potassium can alleviate blood pressure increase caused by high-salt diet and protect the target organs.
出处
《西安交通大学学报（医学版）》
CAS
CSCD
北大核心
2014年第2期157-162,共6页
Journal of Xi’an Jiaotong University（Medical Sciences）
基金
国家重点基础研究发展计划"973"项目(No.2012CB517804)
国家自然科学基金资助项目(No.30671160
81070218)~~
关键词
钠
钾
盐敏感性
肾髓质
转化生长因子-β1
高血压
纤维化
sodium
potassium
salt sensitivity~ renal medulla
transforming growth factor-β1
hypertension fibrosis
