关键词: 过氧化氢, 预处理, PI3K/Akt信号通路, 细胞保护

Abstract: Objective To explore whether PI3K/Akt pathway play a role in H2O2 preconditioning-induced adaptive cytoprotection. Methods setting up the experimental model of H2O2 preconditioning against injury induced by H2O2 at high concentration in cultured PC 12 cells. The viability of cells was measured by MTT assay. The activity of lactate dehydrogenase (LDH) was assessed by colorimetry. The percentage of apoptotic cells was estimated by flow cytometry (FCM) with propidium iodide stain. The levels of akt were detected by Western blot. Results Preconditioning of H2O2 at 100 μmol/L for 90 min significantly protected PC 12 cells from 300 μmol/L H2O2-induced injury, increasing the cell viability from （50.2±4.6）% to（83.8±3.5）% , reducing the activity of LDH from（103±10.21）% to (68.5±5.34)%，and decreasing the rate of apoptotic cells from (65.5±4.1) % to (37.1±2.3) % (P<0.01). H2O2 preconditioning induced expression of p-akt, and ly294002 (an inhibitor of PI3K) blocked expression of p-akt induced by H2O2 preconditioning. Simultaneously ly294002 markedly reduced the anti-cytotoxicity and anti-apoptosis induce by H2O2 preconditioning. Conclusion H2O2 preconditioning induced activation of akt via PI3K-dependent way and activation of PI3K/Akt pathway mediated in adaptive cytoprotection induced by H2O2 precondition.

Key words: hydrogen peroxide, precondition, PI3K/Akt pathway, cytoprotection