Effects and Molecular Mechanism of L-Type Calcium Channel on Fluoride-Induced Kidney Injury

被引:0
作者
Dandan Shao
Jiayong Zhang
Le Tang
Qiuli Yu
Xiaoxiao Hu
Qin Ruan
Wei Ouyang
Zigui Zhang
机构
[1] Zhejiang Normal University,College of Chemistry and Life Science
[2] Zhejiang Normal University,College of Xing Zhi
[3] Zhejiang Normal University,College of Sports and Health Science
来源
Biological Trace Element Research | 2020年 / 197卷
关键词
Fluorosis; Kidney; L-type calcium channel; Apoptosis; Cav1.2;
D O I
暂无
中图分类号
学科分类号
摘要
This study aimed to investigate the role and molecular mechanism of L-type calcium channel (LTCC) on fluoride exposure-induced kidney injury. Subchronic and chronic fluoride exposures were included in the experiment. Each part contained 140 ICR male mice. They were randomly divided into 7 groups: control group, high-fluoride group (NaF 30 mg/L), low-fluoride group (NaF 5 mg/L), high/low-fluoride + agonist (FPL64176) group, high/low-fluoride + inhibitor (nifedipine) group. One week before the end of fluoride exposure, each mouse in the fluoride exposure group was injected intraperitoneally with LTCC agonist (FPL64176) or inhibitor (nifedipine) (5 mg/kg day). The apoptosis of kidney cell was observed by TUNEL, and the protein expression levels of Cav1.2 and CaM, CaMKII, Bcl-2, and Bax were detected by Western blot. Compared with the control group, the protein expression levels of Cav1.2, CaM, and Bax significantly increased, and those of CaMKII and Bcl-2 significantly decreased, the ratio of Bax/Bcl-2 also significantly increased, and the number of apoptotic kidney cells significantly increased in the high/low-fluoride group and in the high/low-fluoride + agonist group. The above indicators and fluoride exposure concentrations showed in time- and dose-dependent changes. Compared with the high/low-fluoride + agonist group, the protein expression level of the molecular in the kidney cells above mentioned was significantly opposite and the number of apoptotic kidney cells significantly decreased in the high/low-fluoride + inhibitor group. In conclusion, LTCC mediates the kidney injury induced by fluoride exposure in mice. Fluoride exposure induced abnormal expression of the Cav1.2 protein, Ca2+ signal transduction pathway, and apoptosis-regulated proteins, which is one of the molecular mechanisms. Nifedipine may be a new and effective anti-fluoride drug.
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页码:213 / 223
页数:10
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