| Project/Area Number |
23592213
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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 |
Orthopaedic surgery
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| Research Institution | Kobe University |
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Principal Investigator |
NISHIYAMA Takayuki 神戸大学, 医学(系)研究科(研究院), 医学研究員 (10379373)
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| Co-Investigator(Kenkyū-buntansha) |
HAYASHI Shinya 神戸大学, 医学部附属病院, 特命助教 (20437487)
FUJISHIRO Takaaki 神戸大学, 医学部附属病院, 特命助教 (50448172)
KANZAKI Niroyuki 神戸大学, 医学部附属病院, 医員 (30514632)
KURODA Ryosuke 神戸大学, 医学研究科, 准教授 (80379362)
KUROSAKA Masahiro 神戸大学, 医学研究科, 教授 (70170115)
NISHIDA Kotaro 神戸大学, 医学部附属病院, 講師 (00379372)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2013: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2012: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2011: ¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
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| Keywords | EPA / 軟骨組織 / アポトーシス / 変形性関節症 / PTEN / 軟骨 / P38MAPK / 軟骨細胞 / p38MAPK / P53R2 |
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| Research Abstract |
Objective: Oxidative stress has been reported to induce apoptosis and degeneration of chondrocytes.But the mechanism of EPA in apoptosis and degeneration of chondrocytes has been unknouwn. We evaluated that the function of EPA on apoptosis and degeneration of chondrocytes.Methods: The expression of MMPs were detected by real-time PCR, and apoptosis related proteins were detected by western blotting and FACS. C57BL/6J mice were used for detecting MMPs expression by immunohistochemistry.Results: EPA inhibited SNP-induced apoptosis of chondrocytes. EPA inhibited SNP-induced expressions of MMP3 and MMP13. The progression of OA was prevented by articular injection of EPA in vivo. Immunohistochemistry demonstrated that MMP3 and MMP13 expression were increased in DMM model. However, intra-articular injection of EPA inhibited the expressions of MMP13. Conclusion: The treatment of EPA can control the oxidative stress-induced OA progression. EPA may be a new therapeutic approach in OA therapy.
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