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吡格列酮激活过氧化物酶体增殖物激活受体-γ可减少人腹膜间皮细胞单核细胞趋化蛋白-1的表达和释放。

Activation of peroxisome proliferator-activated receptor-gamma by glitazones reduces the expression and release of monocyte chemoattractant protein-1 in human mesothelial cells.

机构信息

Medizinische Poliklinik-Innenstadt, Klinikum der Universitaet Muenchen, Muenchen, Germany.

出版信息

Mediators Inflamm. 2012;2012:217696. doi: 10.1155/2012/217696. Epub 2012 Feb 7.

DOI:10.1155/2012/217696
PMID:22496599
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3306974/
Abstract

Human peritoneal mesothelial cells (MC) play an important role in inflammatory processes of the peritoneal cavity by producing various cytokines and chemokines, such as monocyte chemoattractant protein-1 (MCP-1). The present study was designed to assess the effect of the peroxisome proliferator-activated receptor-gamma- (PPARγ-) activator rosiglitazone on the mesothelial MCP-1 expression and release. Primary cultures of MC were obtained from omental tissue. MCP-1 antigen concentrations were measured in the cell supernatant by ELISA and MCP-1 mRNA levels by real-time polymerase chain reaction. The presence of PPARγ on MC was assayed in a Western Blot analysis. MC constitutively express PPARγ. Activation of this receptor via rosiglitazone (0,1-10 μmol/L) resulted in significantly reduced amounts of mesothelial MCP-1 release as well as MCP-1 mRNA. The use of the PPARγ inhibitor GW-9662 could completely prevent the rosiglitazone effects. Rosiglitazone was also effective in reducing TNFα-induced enhanced secretion of MCP-1. Our findings indicate that glitazones are effective in reducing constitutive and TNFα-stimulated mesothelial MCP-1 mRNA expression and release.

摘要

人腹膜间皮细胞（MC）通过产生各种细胞因子和趋化因子，如单核细胞趋化蛋白-1（MCP-1），在腹腔炎症过程中发挥重要作用。本研究旨在评估过氧化物酶体增殖物激活受体-γ-（PPARγ-）激活剂罗格列酮对间皮细胞 MCP-1 表达和释放的影响。从大网膜组织中获得原代 MC 培养物。通过 ELISA 测量细胞上清液中的 MCP-1 抗原浓度，并通过实时聚合酶链反应测量 MCP-1 mRNA 水平。通过 Western Blot 分析检测 MC 上的 PPARγ。MC 持续表达 PPARγ。通过罗格列酮（0、1-10 μmol/L）激活该受体，导致间皮细胞 MCP-1 释放以及 MCP-1 mRNA 的量显著减少。使用 PPARγ 抑制剂 GW-9662 可完全阻止罗格列酮的作用。罗格列酮还可有效降低 TNFα 诱导的 MCP-1 分泌增加。我们的研究结果表明，格列酮类药物可有效降低基础和 TNFα 刺激的间皮细胞 MCP-1 mRNA 表达和释放。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31d3/3306974/fd59e36401cb/MI2012-217696.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31d3/3306974/bf641b7d3168/MI2012-217696.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31d3/3306974/877a02eda6d5/MI2012-217696.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31d3/3306974/1a2b9417f345/MI2012-217696.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31d3/3306974/14245a254a24/MI2012-217696.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31d3/3306974/fd59e36401cb/MI2012-217696.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31d3/3306974/bf641b7d3168/MI2012-217696.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31d3/3306974/877a02eda6d5/MI2012-217696.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31d3/3306974/1a2b9417f345/MI2012-217696.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31d3/3306974/14245a254a24/MI2012-217696.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31d3/3306974/fd59e36401cb/MI2012-217696.005.jpg

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