| 研究課題/領域番号 |
18K15934
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| 研究機関 | 慶應義塾大学 |
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研究代表者 |
尾崎 真理 慶應義塾大学, 医学部(信濃町), 研究員 (90772286)
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| 研究期間 (年度) |
2018-04-01 – 2021-03-31
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| キーワード | Lung stem cells / High fat diet / Fibrosis / Lung cancer |
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| 研究実績の概要 |
In the past year, we have been looking into the effects of a high fat diet (HFD) in relation to specific lung disease such as fibrosis and cancer and have been examining the mechanism by which HFD is associated with these diseases.
Fibrosis study - we have 1) established a quantitative method of analysing fibrosis using the HistoQuest image analysis software, 2) found that HFD causes a significant delay/failure of fibrosis and inflammation resolution, significantly delays AT2 cell proliferation and infiltration of the fibrotic foci, and impairs the contribution of BASCs into epithelial repair.
Cancer study - we have found that tumors in the HFD-fed mice lungs had a significantly higher ratio of proliferating cells and a significant increase of total macrophage number.
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| 現在までの達成度 (区分) |
現在までの達成度 (区分)
2: おおむね順調に進展している
理由
We have completed the bulk of our proposed study and have managed to publish our results. We are now looking more deeply into the mechanisms of the study and are expanding our research by examining the effects of HFD in specific lung diseases.
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| 今後の研究の推進方策 |
Fibrosis study - Want to 1) confirm the mechanism by which HFD is causing a delay in fibrosis repair - may be caused through a switch in energy cellular source from carbohydrates into beta oxidation, therefore, we will block beta oxidation with Etomoxir and observe whether there is return to normal response. 2) identify whether HFD blocks fibrosis resolution completely, or if it only delays. 3) examine the mechanism of fibrosis resolution and show its inhibition in HFD-fed mice by examining MMPs by RT-PCR.
Cancer study - Want to confirm if HFD is causing a higher severity of cancer via a switch in energy cellular source from carbohydrates into beta oxidation, therefore, we will block beta oxidation with Etomoxir and observe whether there is return to normal response.
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