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关节软骨细胞中水通道蛋白4的过表达加剧了佐剂诱导的大鼠关节炎的严重程度：一项[研究类型]和[研究类型]研究。 （你提供的原文中“an and study”部分信息不完整，我只能按现有内容准确翻译）

Overexpression of aquaporin 4 in articular chondrocytes exacerbates the severity of adjuvant-induced arthritis in rats: an and study.

作者信息

Cai Li, Lei Chao, Li Rong, Chen Wei-Na, Hu Cheng-Mu, Chen Xiao-Yu, Li Chun-Mei

机构信息

Department of Pathology, School of Basic Medicine, Anhui Medical University, 81 Meishan Road, Hefei, 230032 Anhui Province China.

School of Pharmacy, Anhui Medical University, 81 Meishan Road, Hefei, 230032 Anhui Province China.

出版信息

J Inflamm (Lond). 2017 Mar 1;14:6. doi: 10.1186/s12950-017-0153-8. eCollection 2017.

DOI:10.1186/s12950-017-0153-8
PMID:28265203
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5333381/
Abstract

BACKGROUND

The dysfunction of articular chondrocytes is a crucial step in rheumatoid arthritis (RA) pathogenesis while its molecular mechanisms are not fully known. This study was aimed to investigate the expression of aquaporin 4 (AQP4) in articular chondrocytes of adjuvant-induced arthritis (AIA) rats and its involvement in AIA development.

METHODS

Thirty rats were divided into normal and AIA group ( = 15). Rat AIA was induced by intradermal injection of complete Freund's adjuvant and evaluated by secondary paw swelling and histological assessments on knee joint damage. Localization and protein expression of AQP4 in articular cartilage were examined by immunohistochemistry and western blot. In vitro study, AIA articular chondrocytes were cultured and treated with acetazolamide, an AQPs inhibitor. AQP4 protein level, cell proliferation and mRNA levels of type-II collagen (COII) and aggrecan were measured by western blot, MTT assay and real-time PCR, respectively.

RESULTS

The results of immunohistochemistry and western blot indicated that AQP4 showed higher protein levels in cartilage tissues of AIA rats than that of normal rats. Correlation analysis revealed that AQP4 protein level in cartilage tissues of AIA rats remarkably correlated positively with secondary paw swelling on day 26 after AIA induction as well as pathological scores on joint damage. Additionally, acetazolamide treatment effectively decreased AQP4 protein level, increased cell proliferation and mRNA levels of COII and aggrecan, suggesting AQP4 inhibition by acetazolamide could normalize the dysfunction of AIA articular chondrocytes in vitro.

CONCLUSIONS

Our data provide certain experimental evidence that AQP4 over-expression in articular chondrocytes aggravated AIA severity and might be a novel target for RA treatment.

摘要

背景

关节软骨细胞功能障碍是类风湿关节炎（RA）发病机制中的关键步骤，但其分子机制尚未完全明确。本研究旨在探讨水通道蛋白4（AQP4）在佐剂性关节炎（AIA）大鼠关节软骨细胞中的表达及其在AIA发病中的作用。

方法

将30只大鼠分为正常组和AIA组（每组15只）。通过皮内注射完全弗氏佐剂诱导大鼠AIA，并通过继发性爪肿胀和膝关节损伤的组织学评估进行评价。采用免疫组织化学和蛋白质印迹法检测AQP4在关节软骨中的定位和蛋白表达。在体外研究中，培养AIA关节软骨细胞并用AQPs抑制剂乙酰唑胺进行处理。分别通过蛋白质印迹法、MTT法和实时PCR检测AQP4蛋白水平、细胞增殖以及Ⅱ型胶原（COII）和聚集蛋白聚糖的mRNA水平。

结果

免疫组织化学和蛋白质印迹结果表明，AIA大鼠软骨组织中AQP4蛋白水平高于正常大鼠。相关性分析显示，AIA诱导后第26天，AIA大鼠软骨组织中AQP4蛋白水平与继发性爪肿胀以及关节损伤的病理评分显著正相关。此外，乙酰唑胺处理有效降低了AQP4蛋白水平，增加了细胞增殖以及COII和聚集蛋白聚糖的mRNA水平，表明乙酰唑胺抑制AQP4可在体外使AIA关节软骨细胞的功能障碍恢复正常。

结论

我们的数据提供了一定的实验证据，即关节软骨细胞中AQP4的过表达加重了AIA的严重程度，可能是RA治疗的新靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/325d/5333381/3db573d96d45/12950_2017_153_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/325d/5333381/e9228c323dfe/12950_2017_153_Fig1_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/325d/5333381/a8ffe26885bb/12950_2017_153_Fig4_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/325d/5333381/0144d4fc2afb/12950_2017_153_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/325d/5333381/569a85b47c1b/12950_2017_153_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/325d/5333381/3db573d96d45/12950_2017_153_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/325d/5333381/e9228c323dfe/12950_2017_153_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/325d/5333381/047bee74e78f/12950_2017_153_Fig2_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/325d/5333381/a8ffe26885bb/12950_2017_153_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/325d/5333381/601d74eb379e/12950_2017_153_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/325d/5333381/0144d4fc2afb/12950_2017_153_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/325d/5333381/569a85b47c1b/12950_2017_153_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/325d/5333381/3db573d96d45/12950_2017_153_Fig8_HTML.jpg

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