| Budget Amount *help |
¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Outline of Final Research Achievements |
In wild type mice, administration of APAP increased intrahepatic expression of chemokines. Despite expression of almost chemokines decreased in 24 h after being increased in 10 h, only CCL3 expression increased up to 24 h. So, we focused on CCL3 and its receptor CCR1, CCR5 in APAP induced liver injury. In histopathological and biochemical analysis, liver injury was relieved in CCL3 deficient and CCR5 deficient mice compared with wild type, however in CCR1 deficient mice, there was no significance in wild type. Also, infiltrate of leucocyte was suppressed in CCL3 deficient and CCR5 deficient mice compared with wild type, but CCR1 deficient has no difference with wild type mice. Further, CCR5 was confirmed to express on the surface of inflammatory cells, such as macrophages, T cells, and NK cells. We suggested the relation of CCL3-CCR5 axis to APAP induced liver injury.
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