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锌对TCP颗粒诱导骨细胞损伤的保护作用     被引量:1

EFFECT OF ZINC ON OSTEOCYTES EXPOSURED TO TRICALCIUMPHOSPHATE PARTICLES

文献类型:期刊文献

中文题名:锌对TCP颗粒诱导骨细胞损伤的保护作用

英文题名:EFFECT OF ZINC ON OSTEOCYTES EXPOSURED TO TRICALCIUMPHOSPHATE PARTICLES

作者:赵旭波[1];张浩杰[1];朱清显[1];张旭俊[1];蔡腾伟[1];张云[1]

机构:[1]绍兴文理学院医学院

年份:2017

卷号:39

期号:1

起止页码:60

中文期刊名:营养学报

外文期刊名:Acta Nutrimenta Sinica

收录:CSTPCD、、北大核心2014、CSCD2017_2018、北大核心、CSCD

基金:浙江省自然科学基金(No.LY17H060007);浙江省中医药科学研究基金计划(No.2012ZB161)

语种:中文

中文关键词:TCP颗粒;ZnTCP颗粒;骨细胞;凋亡;Akt

外文关键词:TCP particles; ZnTCP particles; osteocytes; apoptosis; Akt;

中文摘要:目的观察磷酸三钙(tricalciumphosphate,TCP)颗粒与锌(zinc,Zn)掺杂TCP(Zn TCP)颗粒对骨细胞MLO-Y4活性和功能影响及Zn对TCP颗粒诱导骨细胞损伤的作用。方法骨细胞MLO-Y4分别与TCP颗粒(0.1 mg/ml)和Zn TCP颗粒(0.1 mg/ml)共培养,应用实时荧光定量PCR和Western blot等方法检测Zn干预后骨细胞硬化蛋白SOST(sclerostin)和牙本质基质蛋白1(dentin matrix protein 1,DMP-1)m RNA水平及蛋白表达的变化,研究Zn对TCP磨损颗粒诱导骨细胞功能损伤的影响;通过Calcein-AM标记、MTT和流式细胞术定量分析Zn对TCP颗粒诱导骨细胞活性和凋亡的影响;利用Western blot方法检测Zn干预后骨细胞Akt、phospho-Akt(p-Akt Ser473)和phospho-Akt(p-Akt Thr308)等蛋白的表达变化,探讨Akt信号分子在Zn对TCP颗粒诱导骨细胞损伤保护中的作用,阐明其分子机理。结果 Zn可明显抑制TCP颗粒诱导的骨细胞功能损伤,阻止骨细胞凋亡;同时Zn干预能显著减弱TCP颗粒诱导的骨细胞Akt蛋白失活,表现为上调p-Aktser473和p-Akt Thr308等蛋白表达(P<0.05)。结论 Zn可阻止TCP颗粒诱导的骨细胞损伤,可能与抑制TCP颗粒诱导骨细胞Akt蛋白的失活密切相关。

外文摘要:Objective To observe the effect of tricalciumphosphate (TCP) particles and zinc-containing TCP (ZnTCP) particles on osteocytes MLO-Y4, and to examine the effect of Zn on osteocytes which were injured by TCP paritcles. Methods MLO-Y4 cells and TCP particles (0.1 mg/ml)/ ZnTCP particles (0.1 mg/ml) were co-incubated. The mRNA and protein expressions of SOST and DMP-1 of osteocytes were detected by real-time quantitative PCR and Western blot. Osteocytes injuries were assessed using calcein-AM labeling, MTT assay and the flow cytometry, respectively. The expressions of Akt, phospho-Akt (p-AktSer473) and phospho-Akt (p-AktThr308) of osteocytes were showed by Western blot. Results Zn significantly inhibited TCP particles-induced dysfunction of osteocytes MLO-Y4, and also significantly prevented osteocytes apoptosis (P〈0.05). Furthermore, Zn greatly increased Akt activation which was inhibited by TCP particles, and up-regulated the levels of p-AktSer473 and p-AktThr308 (P〈0.05).Conclusion Zn may prevent TCP particles-induced osteocytes injury, which is mediated by increasing activation of Akt profein in osteocytes MLO-Y4.

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