2016 Fiscal Year Final Research Report
The close-take mechanism between adipose tissue and M1/M2 macrophages after the surgical stress
| Project/Area Number |
26461930
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
General surgery
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| Research Institution | Nippon Medical School |
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Principal Investigator |
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Keywords | M1/M2マクロファージ / 脂肪組織 / 外科的侵襲 / アディポネクチン / PPARγアゴニスト |
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| Outline of Final Research Achievements |
We investigated the effects of PPAR-γ agonist on visceral adipose macrophage population and polarisation in cecal ligation and puncture (CLP) mice. Mice were divided to CLP (C)-group, PPARγ agonist-treated CLP (P)-group, or sham (S)-group. mRNA expressions (iNOS for M1, arginase1 and IL-10 for M2, CD163 and F4/80 for mature macrophages) were quantified by real-time RT-PCR. Tissue sections were subjected to immunohistochemical and TUNEL assay. C-group significantly enhanced arginase1, IL-10 and iNOS mRNA expressions as compared with S-group. P-group significantly increased mRNA level of CD163 and F4/80 in C-group. Increased numbers of CD11b/c- and CD163-positive cells as well as apoptotic cells were observed in C-group. These cells were more abundant in P-group. M1/M2 macrophage activation of adipose tissues is induced in C-group. PPAR-γ agonist may accelerate this activation and recruitment of macrophages, and may restrict adipose tissue inflammation by altering macrophage dynamics.
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| Free Research Field |
医歯薬学
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