High-salt diet accelerates bone loss accompanied by activation of ion channels related to kidney and bone tissue in ovariectomized rats
High-salt diet accelerates bone loss accompanied by activation of ion channels related to kidney and bone tissue in ovariectomized rats
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DOI：
10.1016/j.ecoenv.2022.114024
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发表时间：
2022-08-31
影响因子：
6.8
通讯作者：
Zhu, Xiaofeng
中科院分区：
文献类型：
--
作者：
Cui, Yan;Sun, Kehuan;Zhu, Xiaofeng
盐摄入量过高可诱发多种疾病，如高血压、心血管疾病、肾脏疾病等，也是促进骨吸收的因素之一。高盐饮食导致骨质疏松症加重的机制尚不清楚。本研究采用6月龄去卵巢SD大鼠建立高骨转换模型，然后给予高盐饮食(2.0%w/w氯化钠、8.0%w/w氯化钠)12周，观察高盐饮食对骨代谢的影响。结果表明，高盐饮食可破坏骨微结构，促进尿钙磷排泄，加速骨转换，并可引起肾小管病理结构异常。同时，股骨组织和肾小管上皮细胞钠通道(ENaCα)、电压门控氯通道(ClC)-3表达上调，钠氯协同转运体(NCC)、钠钙交换蛋白(NCX1)表达下调。这些结果证实了高盐饮食可以通过增加骨吸收来破坏骨的微结构，并影响去卵巢大鼠骨组织和肾小管的某些离子通道。
Excessive salt intake can induce a variety of diseases, such as hypertension, cardiovascular disease, kidney disease and so on,it is also one of the factors promoting bone resorption. The mechanism of osteoporosis -induced exacerbations of high salt diet is not well-defined. In this study, we used ovariectomized 6-month-old Sprague Dawley rats to construct a high bone turnover model, and then administrated with high sodium chlo-ride diet (2.0% w/w NaCl, 8.0% w/w NaCl) for 12 weeks to observe the effect of high salt diet on bone meta-bolism. The results showed that high salt diet could lead to the destruction of bone microstructure, promote the excretion of urinary calcium and phosphorus and accelerate the bone turnover, as well as cause the pathologic structural abnormalities in renal tubular. At the same time, it was accompanied by the up-regulated expression of the epithelial sodium channel (ENaC alpha), voltage-gated chloride channels (ClC)-3 and the down-regulated expression of Na-Cl cotransporter (NCC), sodium calcium exchanger (NCX1) in femoral tissue and renal tu-bules. These findings confirm that high salt diet can destroy the microstructure of bone by increasing bone resorption and affect some ion channels of bone tissue and renal tubule in ovariectomized rats.