Short-term exposure to oleandrin enhances responses to IL-8 by increasing cell surface IL-8 receptors.

摘要: Background and Purpose One of the first steps in host defence is migration leukocytes. IL-8 its receptors are a chemokine system essential to such migration. Up-regulation these would be viable strategy treat dysfunctional defence. Here, we studied effects plant glycoside oleandrin on responses human monocytic cell line. Experimental Approach U937 cells were incubated with (1-200 ng mL−1) for either 1 h (pulse) or 24 h (non-pulse). Apoptosis; activation NF-κB, AP-1 NFAT; calcineurin activity (CXCR1 CXCR2) measured using Western blotting, RT-PCR reporter gene assays. Key Results Pulse exposure did not induce apoptosis cytoxicity as observed after non-pulse exposure. Pulse enhanced NF-κB induced by but that TNF-α, IL-1, EGF LPS. Exposure other apoptosis-inducing compounds (azadirachtin, resveratrol, thiadiazolidine, benzofuran) enhance NF-κB. increased expression chemotaxis, release enzymes NFAT along IL-8-mediated activation, wound healing. numbers surface receptors. Conclusions Implications Short-term (1 h; pulse) toxic oleandrin, biological cells, without cytoxicity. could provide therapy those conditions where leukocyte defective.