Oxidative stress and coronary artery lesion in Kawasaki disease
| Project/Area Number |
23791195
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Pediatrics
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| Research Institution | Tokai University |
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Principal Investigator |
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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 |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2013: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2012: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2011: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 川崎病冠動脈炎 / LCWE / 酸化ストレス / Nrf2遺伝子 / Keap1遺伝子 / 川崎病 / アポトーシス |
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| Research Abstract |
Nrf2 is essential to the expression of antioxidant genes. Involvement of oxidative stress in the development of coronary arteritis(CA) in Kawasaki disease(KD) remains unknown. We have tested whether the disruption of Nrf2 in mice causes exacerbated CA in a murine model of KD induced by Lactobacillus casei cell wall extract(LCWE). Six week-old male Nrf2 knockout(KO) and wild type (WT) mice were injected with either PBS or 300ug of LCWE. Two and 4 weeks after LCWE administration, severity of CA was assessed. KO mice had decreased mRNA expression of antioxidant genes, including Ho-1 and NQO1. In contrast to our hypothesis, KO mice showed less severe CA. Serum cytokine levels such as TNFalpha, IL1beta, IL6 and MCP1 were lower in KO than WT mice. Spleen from KO mice exhibited increased number of apoptotic cells. These results suggest that, although Nrf2 induces antioxidant genes (benefit), it suppresses apoptosis of inflammatory cells, leading to exacerbation of CA (risk) in KD.
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Report
(4 results)
Research Products
(1 results)
