The role of heme-oxygenase-1 in pathogenesis of cerebral malaria in the co-culture model of human brain microvascular endothelial cell and ITG Plasmodium falciparum-infected red blood cells
10.1016/j.apjtm.2016.11.011
- Author:
Pimwan THONGDEE
1
;
Kesara NA-BANGCHANG
1
;
Kesara NA-BANGCHANG
2
Author Information
1. Graduate Program in Bioclinical Sciences, Chulabhorn International College of Medicine, Thammasat University
2. Center of Excellence in Pharmacology and Molecular Biology of Malaria and Cholangiocarcinoma, Thammasat University
- Publication Type:Journal Article
- Keywords:
Co-protoporphyrin inducer;
Heme-oxygenase-1;
Human brain microvascular endothelial cell;
Plasmodium falciparum;
Zn(Ⅱ)-protoporphyrin inhibitor
- From:
Asian Pacific Journal of Tropical Medicine
2017;10(1):20-24
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the role of human host heme-oxygenase-1 (HO-1) in pathogenesis of cerebral malaria in the in vitro model. Methods The effect of human host HO-1 [human brain microvascular endothelial cell (HBMEC)] on hemoglobin degradation in the co-culture model of HBMEC and ITG Plasmodium falciparum-infected red cells (iRBC) through measurement of the enzymatic products iron and bilirubin. Results Following exposure to the HO-1 inducer CoPPIX at all concentrations, the HBMEC cells apoptosis occurred, which could be prominently observed at 15 μM of 3 h exposure. In contrast, there was no significant change in the morphology in the non-exposed iRBC at all concentrations and exposure time. This observation was in agreement with the levels of the enzymatic degradation products iron and bilirubin, of which the highest levels (106.03 and 1753.54% of baseline level, respectively) were observed at 15 μM vs. 20 μM at 3 h vs. 24 h exposure. For the effect of the HO-1 inhibitor ZnPPIX, HBMEC cell morphology was mostly unchanged, but significant inhibitory effect on cell apoptosis was seen at 10 μM for the exposure period of 3 h (37.17% of baseline level). The degree of the inhibitory effect as reflected by the level of iron produced was not clearly observed (highest effect at 10 μM and 3 h exposure). Conclusions Results provide at least in part, insight into the contribution of HO-1 on CM pathogenesis and need to be confirmed in animal model.
