Relationship between p38MAPK signaling pathway and lipopolysaccharide-induced mitochondrial fission in alveolar epithelial cells: an in vitro experiment

Objective To evaluate the relationship between p38 mitogen-activated protein kinase (p38MAPK) signaling pathway and lipopolysaccharide (LPS)-induced mitochondrial fission in alveolar epithelial cells using an in vitro experiment. Methods The cultured alveolar epithelial cells were subcultured and seeded in 96-well plates at the density of 2 × 105 cells/ml (200 μl/well). The cells were divided into 4 groups (n=10 each) when cell confluence reached 80% using a random number table method: control group (group C), LPS group, LPS+ SB203580 group (group LPS+ SB) and LPS+ dimethyl sulfoxide (DMSO) group.Cells were incubated with LPS 10 μg/ml for 24 h in group LPS.Cells were incubated with p38MAPK inhibitor SB203580 10 μmol (dissolved in DMSO) for 1 h and then with LPS 10 μg/ml for 24 h in group LPS+ SB.Cells were incubated with the equal volume of DMSO for 1 h and then with LPS 10 μg/ml for 24 h in group LPS+ DMSO.Malonaldehyde (MDA) content and superoxide dismutase (SOD) activity were measured.The expression of phosphorylated p38MAPK (p-p38MAPK), heme oxygenase-1 (HO-1), dynamin-related protein 1 (DRP1) and fission protein 1 (FIS1) was determined by Western blot. Results Compared with group C, the MDA content was significantly increased, the SOD activity was decreased, and the expression of p-p38MAPK, HO-1, FIS1 and DRP1 was up-regulated in LPS, LPS+ SB and LPS+ DMSO groups (P 0.05). Conclusion The p38MAPK signaling pathway activation can up-regulate the expression of HO-1, thus reducing LPS-induced mitochondrial fission in alveolar epithelial cells. Key words: P38 mitogen-activated protein kinase; Lipopolysaccharide; Epithelial cells; Mitochondrial fission