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高盐饮食加速去卵巢大鼠的骨丢失,伴有与肾脏和骨组织相关的离子通道激活。

High-salt diet accelerates bone loss accompanied by activation of ion channels related to kidney and bone tissue in ovariectomized rats.

机构信息

The First Affiliated Hospital of Jinan University, Guangzhou, Guangdong 510630, PR China; School of Traditional Chinese Medicine, Jinan University, Guangzhou, Guangdong 510630, PR China.

The First Affiliated Hospital of Shenzhen University,Shenzhen Second People's Hospital, Shenzhen, Guangdong 518020, PR China.

出版信息

Ecotoxicol Environ Saf. 2022 Oct 1;244:114024. doi: 10.1016/j.ecoenv.2022.114024. Epub 2022 Aug 31.

DOI:10.1016/j.ecoenv.2022.114024
PMID:36057202
Abstract

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 chloride diet (2.0% w/w NaCl, 8.0% w/w NaCl) for 12 weeks to observe the effect of high salt diet on bone metabolism. 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 (ENaCα), 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 tubules. 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.

摘要

过量的盐摄入会引起多种疾病,如高血压、心血管疾病、肾病等,也是促进骨吸收的因素之一。高盐饮食导致骨质疏松症恶化的机制尚不清楚。在本研究中,我们使用 6 月龄去卵巢 Sprague Dawley 大鼠构建高骨转换模型,然后给予高氯化钠饮食(2.0% w/w NaCl,8.0% w/w NaCl)12 周,观察高盐饮食对骨代谢的影响。结果表明,高盐饮食可导致骨微结构破坏,促进尿钙磷排泄和骨转换加速,并导致肾小管病理性结构异常。同时,伴随着股骨组织和肾小管中上皮钠通道(ENaCα)、电压门控氯离子通道(ClC)-3 的表达上调,以及钠-氯共转运蛋白(NCC)、钠钙交换器(NCX1)的表达下调。这些发现证实,高盐饮食通过增加骨吸收破坏骨微结构,并影响去卵巢大鼠骨组织和肾小管中的一些离子通道。

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