Triptolide inhibits the Apoptosis and Reactive Oxygen Species Production in Hydrogen Peroxide-Treated Nasal Epithelial Cells by Regulating PTEN/PI3K/AKT Signaling Pathway

Abstract

Wang et al.: Triptolide inhibits the Nasal Epithelial CellsChronic rhinosinusitis is a chronic inflammatory condition that caused by many factors. However, the underlying mechanism of chronic rhinosinusitis remains unclear. The current study focused on the roles of triptolide on hydrogen peroxide treated nasal epithelial cells and the underling mechanism. Hydrogen peroxide treated human nasal epithelial cells were cultured and treated by different concentrations of triptolide, cell growth and cell death were determined by cell counting kit-8 and flow cytometry methods. Moreover, effects of triptolide on expression of superoxide dismutase as well as malondialdehyde in nasal epithelial cells treated by hydrogen peroxide were evaluated by enzyme-linked immunosorbent assay analysis. Furthermore, effects of triptolide on expression of phosphatase and tensin homolog deleted on chromosome 10/phosphatidylinositol 3-kinase/protein kinase B molecules in hydrogen peroxide treated nasal epithelial cells have been examined by Western blot method. We found treatment of hydrogen peroxide markedly inhibited growth of the nasal epithelial cells in dose-dependent manner and triptolide could reverse the effect induced by hydrogen peroxide. Moreover, triptolide significantly decreased the apoptosis of the nasal epithelial cells induced by hydrogen peroxide in dose-dependent manner; moreover, triptolide reduced superoxide dismutase as well as malondialdehyde levels in dose dependent manner. Finally, triptolide downregulated phosphatase and tensin homolog deleted on chromosome 10 and upregulated the phosphatidylinositol 3-kinase related signalling in hydrogen peroxide treated cells in vitro. In conclusion, triptolide may exert anti-apoptotic and anti-oxidative behaviors in chronic rhinosinusitis via affecting phosphatase and tensin homolog deleted on chromosome 10/phosphatidylinositol 3-kinase/protein kinase B signaling. The results of current work study may provide new evidence for the research as well as management of chronic rhinosinusitis.