Salt-induced epithelial-to-mesenchymal transition in Dahl salt-sensitive rats is dependent on elevated blood pressure.
Salt-induced epithelial-to-mesenchymal transition in Dahl salt-sensitive rats is dependent on elevated blood pressure.
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Dahl 盐敏感大鼠中盐诱导的上皮间质转变依赖于血压升高。
DOI：
10.1590/1414-431x20133554
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发表时间：
2014-02
期刊：
影响因子：
--
通讯作者：
Yuan ZY
中科院分区：
文献类型：
--
作者：
Wang Y;Mu JJ;Liu FQ;Ren KY;Xiao HY;Yang Z;Yuan ZY
膳食盐摄入量与高血压和心血管疾病有关。越来越多的证据表明，对盐敏感的人摄入高盐更容易患上肾纤维化。上皮间质转化（EMT）参与人类和动物肾纤维化的发生和进展。本研究的目的是调查高盐饮食对 Dahl 盐敏感 (SS) 大鼠 EMT 的影响。 24 只雄性 SS 和体型 SS-13BN 大鼠被随机分为正常饮食或高盐饮食。 4周后，分析收缩压（SBP）和蛋白尿，并对肾纤维化进行组织病理学评估。使用免疫组织化学和 E-钙粘蛋白和 α 平滑肌肌动蛋白 (α-SMA) 实时 PCR 评估肾小管 EMT。 4周后，SS高盐组的收缩压和蛋白尿明显高于正常饮食组。 SS 大鼠中 E-钙粘蛋白表达减少和 α-SMA 表达增强表明，膳食盐摄入诱导肾纤维化和肾小管 EMT。血压和肾间质纤维化均与E-cadherin呈负相关，与α-SMA呈正相关。盐摄入引起SS大鼠肾小管EMT和肾损伤，这种关系可能取决于血压升高。
Dietary salt intake has been linked to hypertension and cardiovascular disease. Accumulating evidence has indicated that salt-sensitive individuals on high salt intake are more likely to develop renal fibrosis. Epithelial-to-mesenchymal transition (EMT) participates in the development and progression of renal fibrosis in humans and animals. The objective of this study was to investigate the impact of a high-salt diet on EMT in Dahl salt-sensitive (SS) rats. Twenty-four male SS and consomic SS-13BN rats were randomized to a normal diet or a high-salt diet. After 4 weeks, systolic blood pressure (SBP) and albuminuria were analyzed, and renal fibrosis was histopathologically evaluated. Tubular EMT was evaluated using immunohistochemistry and real-time PCR with E-cadherin and alpha smooth muscle actin (α-SMA). After 4 weeks, SBP and albuminuria were significantly increased in the SS high-salt group compared with the normal diet group. Dietary salt intake induced renal fibrosis and tubular EMT as identified by reduced expression of E-cadherin and enhanced expression of α-SMA in SS rats. Both blood pressure and renal interstitial fibrosis were negatively correlated with E-cadherin but positively correlated with α-SMA. Salt intake induced tubular EMT and renal injury in SS rats, and this relationship might depend on the increase in blood pressure.