Aspirin-triggered Lipoxin A₄Induces The Expression Of Heme Oxidase-1in Microglia

Objective:To discuss whether the expression of heme oxidase-1is induced by aspirin-triggered lipoxin A4in microglia, and investigate the possible mechanism.Methods:In our pre-experiment, we found that the expression of pAkt was increased obviously by treating100nM ATL in murine BV2cells. So, this experiment was grouped as follow to investigated whether the enhanced expression of pAkt was related to the effect of ATL on HO-1. Groups:(1)Control group:Treat BV2cells with serum-free culture medium(DMEM);(2)Group of Boc-2:Pretreat BV2cells with20μM Boc-2for1hour;(3)Group of LY294002:Pretreat BV2cells with20μM LY294002for1hour;(4)Group of ATL:Add ATL to make sure the final concentration of ATL is100nM;(5) Add ATL to make sure the final concentration of ATL is100nM after the pretreatment of20μM Boc-2for1hour;(6)Add ATL to make sure the final concentration of ATL is100nM after the pretreatment of20μM LY294002for1hour.Results:Western Blot showed that the phosphorylation of Akt was up-regulated after adding100nM ATL in the culture medium of BV2cells for1hour, and Boc-2or LY294002could reverse this effect respectively. Moreover, the expression of Nrf2showed this protein could translocate from cytoplasm to the nuclei by adding100nM ATL in the culture medium of BV2cells for2hours. However, if we pretreated BV2cells with Boc2or LY294002for1hour, the translocation of Nrf2would be suppressed. Treating BV2cells with100nM for24hours,it was not difficult to find out the expression of HO-1was raised obviously, while this effect was repressed by Boc-2and LY294002, and there was almost no change for expression of HO-1when only using Boc-2or LY294002. Conclusion:ATL may induce the expression of HO-1in BV2cells, which may be involved with PI3K/Akt activation and Nrf2translocation.