| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2012: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Outline of Final Research Achievements |
During acute lung inflammation, the lung microvasculature becomes hyperpermeable, resulting in immune cell infiltration and tissue edema. In this study, we examined the effects n-3 PUFAs onlung microvascular cell permeability.Human lung microvascular endothelial cells (HMVEC-L) were seeded on fibronectin-coated transwell inserts. The cells were pretreated with docosahexaenoic acid (DHA) or eicosapentaenoic acid (EPA) (n-3 PUFAS), and then treated with LPS to simulate acute lung injury. Pretreatment with DHA and EPA prior to LPS stimulation significantly attenuated LPS-induced cell permeability. EPA decreased histamine receptor 1 (H1R) and mRNA expression following LPS stimulation. Interleukin (IL)-6 mRNA expression in response to LPS treatment was significantly reduced by both DHA and EPA pretreatment. DHA and EPA attenuated LPS-induced lung microvascular endothelial cell permeability through a mechanism that may involve IL-6. EPA pretreatment may influence H1R expression.
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