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- Title
低浓度CO 暴露促进大鼠肝前体细胞增殖的体外研究.
- Authors
何大立; 张玄; 慕喜喜; 蒲猛; 黄启科; 赵戈; 陶开山
- Abstract
Objective: To explore the role and molecular mechanism of hepatic progenitor cell (HPC) exposed to low-concentration exogenous CO molecular against relative nutrition deficiency. Methods: HPCs (WB-F344) were cultured in vitro in 10%FBS and 4% FBS medium respectively. Meanwhile, inactive CORM-2 (iCORM-2) and CORM-2 were administered respectively to different groups of WB-F344 cultured in 4%FBS medium. 100 μM was chosen as the same CO exposure concentration both in iCORM-2 and CORM-2 groups. Cell viability and proliferation were observed in all groups. Acridine orange (AO) staining was used to detect the formation of Acidic autophagosomes in WB-F344 cells. The transformation between LC3-I and LC3-II was detected with western-blot. WB-F344 cells exhibited an exponential growth in 10%FBS medium and achieved growth peak in the fifth day. On the contrary, WB-F344 cells showed an inhibitory viability and very slow growth rate in 4% FBS medium. The proliferative cell number decreased at the same time point compared to the control group. While exposed to 100 μM CORM-2, WB-F344 cells' viability and growth situation improved significantly and had an increased growth peak. AO staining displayed obvious orange fluorescent in WB-F344 cells cultured in 4%FBS mediumand the intensity of orange fluorescent enhanced after CO molecular exposure. Western-blot assay demonstrated that relative nutrition deficiency (4%FBS) promoted LC3-I to transform into LC3-II in the growth of WB-F344 cells. CO molecular exposure increased the production of LC3-II and the ratio between LC3-II and LC3-I (P<0.05). Further western-blot detection revealed that the expression of p-AKT and mTOR declined simultaneously in the CO exposure process in concurrence with the increased expression of HO-1. Low-concentration CO exposure could benefit the autophagy formation in WB-F344 cell against severe environment and promote its viability and proliferation. The molecular mechanism referred to AKT/mTOR signal pathway inhibition and HO-1 increase.
- Publication
Progress in Modern Biomedicine, 2017, Vol 17, Issue 9, p1601
- ISSN
1673-6273
- Publication type
Article
- DOI
10.13241/j.cnki.pmb.2017.09.001