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氟化钠（NaF）通过内质网（ER）应激途径诱导脾脏细胞凋亡 并且 。 你提供的原文似乎不太完整，最后的“and.”后面应该还有内容。

Sodium fluoride (NaF) induces the splenic apoptosis via endoplasmic reticulum (ER) stress pathway and .

作者信息

Deng Huidan, Kuang Ping, Cui Hengmin, Chen Lian, Luo Qin, Fang Jing, Zuo Zhicai, Deng Junliang, Wang Xun, Zhao Ling

机构信息

College of Veterinary Medicine, Sichuan Agricultural University, Ya'an 625014, China.

Key Laboratory of Animal Diseases and Environmental Hazards of Sichuan Province, Ya'an 625014, China.

出版信息

Aging (Albany NY). 2016 Dec 27;8(12):3552-3567. doi: 10.18632/aging.101150.

DOI:10.18632/aging.101150
PMID:28039491
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5270686/
Abstract

At present, there are no reports on the relationship between fluoride-induced apoptosis and endoplasmic reticulum (ER) stress (ER stress) in the spleen of human and animals and . Therefore, the aim of this study was to define sodium fluoride (NaF)-induced apoptosis mediated by ER stress in the spleen of mice and . Apoptosis and expression levels of the ER stress-related proteins were detected by flow cytometry and western blot, respectively. The results showed that NaF treatment increased lymphocytes apoptosis, which was consistent with NaF-caused ER Stress. NaF-caused ER stress was characterized by up-regulating protein expression levels of glucose-regulated protein 78 (BiP) and glucose-regulated protein 94 (GRP94), and by activating unfolded protein response (UPR). The signaling pathway of ER stress-associated apoptosis was activated by up-regulating protein expression levels of cleaved cysteine aspartate specific protease-12 (cleaved caspase-12), growth arrest and DNA damage-inducible gene 153 (Gadd153/CHOP) and phosphorylation of JUN N-terminal kinase (p-JNK). Additionally, our study found that apoptotic rate was decreased with remarkable down-regulation of the cleaved caspase-12, CHOP, p-JNK after ER stress was inhibited by 4-Phenylbutyric acid (4-PBA) treatment. In conclusion, NaF-induced apoptosis may mediated by ER stress in the spleen.

摘要

目前，关于人和动物脾脏中氟诱导的细胞凋亡与内质网（ER）应激之间的关系尚无报道。因此，本研究的目的是确定氟化钠（NaF）诱导的内质网应激介导的小鼠脾脏细胞凋亡。分别通过流式细胞术和蛋白质印迹法检测细胞凋亡和内质网应激相关蛋白的表达水平。结果表明，NaF处理增加了淋巴细胞凋亡，这与NaF引起的内质网应激一致。NaF引起的内质网应激表现为上调葡萄糖调节蛋白78（BiP）和葡萄糖调节蛋白94（GRP94）的蛋白表达水平，并激活未折叠蛋白反应（UPR）。内质网应激相关凋亡的信号通路通过上调半胱天冬酶-12（cleaved caspase-12）、生长停滞和DNA损伤诱导基因153（Gadd153/CHOP）的蛋白表达水平以及JUN氨基末端激酶（p-JNK）的磷酸化而被激活。此外，我们的研究发现，在用4-苯基丁酸（4-PBA）处理抑制内质网应激后，cleaved caspase-12、CHOP、p-JNK显著下调，凋亡率降低。总之，NaF诱导的凋亡可能是由脾脏中的内质网应激介导的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ea3/5270686/57dd257e99e1/aging-08-3552-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ea3/5270686/13b43b7d9ace/aging-08-3552-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ea3/5270686/08d18a11e78c/aging-08-3552-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ea3/5270686/81764887dce6/aging-08-3552-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ea3/5270686/f2303f6c5370/aging-08-3552-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ea3/5270686/2d27d03b8bd3/aging-08-3552-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ea3/5270686/d1cd90407fa1/aging-08-3552-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ea3/5270686/95765777f84d/aging-08-3552-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ea3/5270686/5ca108f1060d/aging-08-3552-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ea3/5270686/cda2466f131b/aging-08-3552-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ea3/5270686/57dd257e99e1/aging-08-3552-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ea3/5270686/13b43b7d9ace/aging-08-3552-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ea3/5270686/08d18a11e78c/aging-08-3552-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ea3/5270686/81764887dce6/aging-08-3552-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ea3/5270686/f2303f6c5370/aging-08-3552-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ea3/5270686/2d27d03b8bd3/aging-08-3552-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ea3/5270686/d1cd90407fa1/aging-08-3552-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ea3/5270686/95765777f84d/aging-08-3552-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ea3/5270686/5ca108f1060d/aging-08-3552-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ea3/5270686/cda2466f131b/aging-08-3552-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ea3/5270686/57dd257e99e1/aging-08-3552-g010.jpg

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