Nitric oxide-induced autophagy and the activation of activated protein kinase pathway protect against apoptosis in human dental pulp cells

摘要: Aim To investigate the role of nitric oxide (NO)-induced autophagy in human dental pulp cells (HDPCs) and involvement AMP-activated protein kinase (AMPK) pathway. Methodology The MTT assay was used to determine cytotoxic effect NO donor sodium nitroprusside (SNP) HDPCs. Apoptosis detected by means terminal deoxynucleotidyl transferase dUTP nick-end labelling (TUNEL) assay, apoptosis- or autophagy-related signal molecules were observed Western blot analysis. Acidic autophagolysosomal vacuoles stained with acridine orange detect presence 3-methyladenine (3MA) inhibit autophagy. To explore mechanism underlying its protective against apoptosis, compound C, chemical AMPK inhibitor, used. Statistical analysis performed using Student's t-test variance (anova) followed Student–Newman–Keuls test (P < 0.05). Results SNP decreased viability HDPCs a dose- time-dependent manner. Exposing SNP increased levels p62 LC3-II, typical markers autophagy, number acidic vacuoles, indicating appearance as staining (P < 0.05). Pre-treatment 3MA cell but cleaved poly(ADP-ribose) polymerase (PARP) caspase-3, apoptosis indicators, SNP-treated activated AMPK/ULK signalling, whilst inhibition C enhanced apoptotic death induced (P < 0.05). Conclusion NO activation, which plays survival NO-induced apoptosis.