Effects of heme oxygenase-1 preconditioning on oxidative damage in alveolar epithelial type Ⅱ cells in rats
10.3760/cma.j.issn.0254-1416.2010.11.027
- VernacularTitle:血红素加氧酶-1预处理对大鼠肺泡Ⅱ型上皮细胞氧化损伤的影响
- Author:
Hongmin WANG
;
Mingjiang QIAN
;
Miao CHEN
;
Yan WU
- Publication Type:Journal Article
- Keywords:
Heme oxygenase-1;
.Epithelial cells;
Hydrogen peroxide
- From:
Chinese Journal of Anesthesiology
2010;30(11):1372-1374
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effects of heme oxygenase-1 (HO-1) preconditioning on oxidative damage in alveolar epithelial type Ⅱ (AE- Ⅱ) cells in rats. Methods The primarily cultured AE- Ⅱ cells isolated from male SD rats were randomly assigned to one of 6 groups (n = 8 each): control group (group C),H2O2 group and 4 different concentrations of HO-1 preconditioning group (group H1-4). The cells were continuously incubated for 5 h in group C. H2O2 0.5 mmol/L was added and the cells were incubated for3 h in group H2O2.In group H1-4, HO-1 0.01, 0.10, 1.00 and 10.00 μmol/L were added and the cells were incubated for2 h, then H2O2 0.5 mmol/L was added and the cells were incubated for 3 h. After the end of incubation, the cell morphology was observed under inverted phase contrast microscope, the AE- Ⅱ cells were counted, and the cell viability was determincd. Results The most AE- Ⅱ cells were adherent and round, had homogeneous cytoplasm, and the cytoplasm contains granular materials in group C and H2-4, while the vacuoles appeared in AE- Ⅱ cells and the cell debris appearecd in the supernatant in group H2 O2 and H1 . Compared with group C, the cell count and cell viability were significantly decreased in group H2 O2 and H1 (P ＜ 0.05). Compared with group H2 O2 and H1, the cell count and cell viability were significantly increased in group H2-4 (P ＜ 0.05). There was no significant difference in the cell count and cell viability between group H2O2 and H1, and among group H2～4(P ＞ 0.05) .Conclusion Preconditioning with 0.10-10.00 μmol/L HO-1 can reduce oxidative damage in rat AE- Ⅱ cells.
