Nitric oxide induces apoptosis in mouse thymocytes.

摘要: Nitric oxide (NO) produced at high concentrations by the inducible NO synthase is an important effector molecule involved in immune regulation and defense. We have examined whether represents a signal for triggering apoptosis thymocytes. Freshly isolated thymocytes were incubated with different chemical donors various intervals. Apoptosis was determined detection of DNA strand breaks situ nick translation. All induced thymocyte 30% positive vs 10% controls after 8 h. prevented addition ZnSO4. Short-term pre-exposure to resulted protection from glucocorticoids comparable protective effect heat shock. Flow cytometry revealed that treatment as well shock or dexamethasone incubation accompanied reduction CD4+ CD8+ subpopulation. induction increased expression p53, detected PCR analysis 2 h donor addition. In vivo mice endotoxin results thymic apoptosis. Focal found occur close proximity blood vessels 18 LPS treatment. Capillary endothelium dendritic cells adjacent apoptotic foci stain strongly expression. Furthermore, vitro experiment using cocultures LPS/cytokine-activated endothelial expressing synthase, significantly rate found, this could be completely inhibiting production. Addition these did not lead further increase percentage thymocytes, underlining on dexamethasone-induced