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环孢素A和血管紧张素II在人牙龈成纤维细胞中增加晚期氧化蛋白产物生成的体外研究

Increased Advanced Oxidation Protein Products Generation by Cyclosporine-A and Angiotensin II in Human Gingival Fibroblasts - Ex-vivo Study.

作者信息

Ranga Rao Suresh, Subbarayan Rajasekaran, Ajitkumar Supraja, Murugan Girija Dinesh

机构信息

Head of Department, Department of Periodontics, Sri Ramachandra University , Chennai, Tamil Nadu, India .

Research Scholar, Centre for Regenerative Medicine and Stem Cell Research, Central Research Facility, Sri Ramachandra University , Chennai, Tamil Nadu, India .

出版信息

J Clin Diagn Res. 2017 Jan;11(1):ZC49-ZC52. doi: 10.7860/JCDR/2017/22246.9183. Epub 2017 Jan 1.

DOI:10.7860/JCDR/2017/22246.9183
PMID:28274044
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5324495/
Abstract

INTRODUCTION

Cyclosporin-A (CsA), an immunosuppressant, induces renal fibrosis and Renin Angiotensin System (RAS) is known to play a major role. CsA has the potential to increase the oxidative stress; specifically through the Advanced Oxidation Protein Products (AOPP) which could possibly stimulate fibrosis. A similar type of pathology occurs even in the gingiva known as CsA Induced Gingival Overgrowth (CIGO).

AIM

This study was undertaken to estimate the AOPP generation by Human Gingival Fibroblasts (HGF) under the influence of CsA and Angiotensin II (Ang II).

MATERIALS AND METHODS

Six healthy gingival tissue samples were obtained during crown lengthening procedure and primary HGF were cultured using enzymatic digestion method. The ideal non-cytotoxic concentrations of CsA and Ang II were identified using cytotoxicity assay. Later, HGF were incubated with CsA and Ang II for 12 hours and AOPP assay was performed at zero and one hour interval.

RESULTS

There was a statistically significant increase in AOPP production in both the CsA and Ang II when compared to the control group with a p value<0.05.

CONCLUSION

CsA can induce oxidative stress and preventing/controlling it may be necessary to prevent untoward effect of the drug.

摘要

引言

环孢素A(CsA)是一种免疫抑制剂,可诱导肾纤维化,已知肾素血管紧张素系统(RAS)在其中起主要作用。CsA有可能增加氧化应激;具体是通过晚期氧化蛋白产物(AOPP),其可能刺激纤维化。即使在牙龈中也会出现类似类型的病理情况,称为CsA诱导的牙龈过度生长(CIGO)。

目的

本研究旨在评估在CsA和血管紧张素II(Ang II)影响下,人牙龈成纤维细胞(HGF)产生AOPP的情况。

材料与方法

在牙冠延长术期间获取6份健康牙龈组织样本,采用酶消化法培养原代HGF。使用细胞毒性试验确定CsA和Ang II的理想无细胞毒性浓度。随后,将HGF与CsA和Ang II孵育12小时,并在0小时和1小时间隔进行AOPP检测。

结果

与对照组相比,CsA组和Ang II组的AOPP产量均有统计学显著增加,p值<0.05。

结论

CsA可诱导氧化应激,预防/控制氧化应激可能对于预防该药物的不良影响是必要的。

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本文引用的文献

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Dent Res J (Isfahan). 2016 Sep;13(5):405-412. doi: 10.4103/1735-3327.192276.
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Optimisation of an Advanced Oxidation Protein Products Assay: Its Application to Studies of Oxidative Stress in Diabetes Mellitus.高级氧化蛋白产物检测方法的优化:其在糖尿病氧化应激研究中的应用
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Advanced oxidation protein products induce hypertrophy and epithelial-to-mesenchymal transition in human proximal tubular cells through induction of endoplasmic reticulum stress.高级氧化蛋白产物通过诱导内质网应激,在人近端肾小管细胞中诱导肥大和上皮-间质转化。
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Nox2 is a mediator of chronic CsA nephrotoxicity.NOX2 是慢性 CsA 肾毒性的介质。
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