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氟对大鼠硬组织超微结构及I型胶原蛋白表达的影响。

Effects of fluoride on the ultrastructure and expression of Type I collagen in rat hard tissue.

作者信息

Yan Xiaoyan, Hao Xianhui, Nie Qingli, Feng Cuiping, Wang Hongwei, Sun Zilong, Niu Ruiyan, Wang Jundong

机构信息

Shanxi Key Laboratory of Ecological Animal Science and Environmental Veterinary Medicine, Shanxi Agricultural University, Taigu, Shanxi 030801, People's Republic of China; Department of Biology, Taiyuan Normal University (TYNU), Taiyuan 030031, People's Republic of China.

Department of Biology, Taiyuan Normal University (TYNU), Taiyuan 030031, People's Republic of China.

出版信息

Chemosphere. 2015 Jun;128:36-41. doi: 10.1016/j.chemosphere.2014.12.090. Epub 2015 Feb 2.

Abstract

Long-term excessive fluoride (F) intake disrupts the balance of bone deposition and remodeling activities and is linked to skeletal fluorosis. Type I collagen, which is responsible for bone stability and cell biological functions, can be damaged by excessive F ingestion. In this study, Sodium fluoride (NaF) was orally administrated to rat at 150 mg L(-1) for 60 and 120 d. We examined the effects of excessive F ingestion on the ultrastructure and collagen morphology of bone in rats by using transmission electron microscopy (TEM). Furthermore, we investigated the effect of F consumption on the expression levels of COL1A1 and COL1A2 in the bone tissues of rats by using quantitative real time (qRT)-PCR, to elucidate the molecular mechanisms of F-induced collagen protein damage. Our results showed that F affected collagen I arrangement and produced ultrastructural changes in bone tissue. Meanwhile, the mRNA expression of COL1A1 and COL1A2 were reduced and the COL I protein levels decreased in the fluorosis group. We concluded that excessive F ingestion adversely affected collagen I arrangement and caused ultrastructural changes in bone tissue. Reduced COL1A1 mRNA expression and altered COL I protein levels may contribute to the skeletal damage resulting from F exposure.

摘要

长期过量摄入氟化物(F)会破坏骨沉积与重塑活动的平衡,并与氟骨症相关。负责骨骼稳定性和细胞生物学功能的I型胶原蛋白会因过量摄入氟而受损。在本研究中,以150 mg L(-1)的剂量给大鼠口服氟化钠(NaF),持续60天和120天。我们使用透射电子显微镜(TEM)研究了过量摄入氟对大鼠骨骼超微结构和胶原形态的影响。此外,我们通过定量实时(qRT)-PCR研究了氟摄入对大鼠骨组织中COL1A1和COL1A2表达水平的影响,以阐明氟诱导胶原蛋白损伤的分子机制。我们的结果表明,氟影响I型胶原排列并在骨组织中产生超微结构变化。同时,氟骨症组中COL1A1和COL1A2的mRNA表达降低,COL I蛋白水平下降。我们得出结论,过量摄入氟会对I型胶原排列产生不利影响,并导致骨组织超微结构变化。COL1A1 mRNA表达降低和COL I蛋白水平改变可能导致氟暴露引起的骨骼损伤。

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