NO/cGMP/PKG activation protects Drosophila cells subjected to hypoxic stress.

摘要: Abstract The anoxia-tolerant fruit fly, Drosophila melanogaster, has routinely been used to examine cellular mechanisms responsible for anoxic and oxidative stress resistance. Nitric oxide (NO), an important signaling molecule, its downstream activation of cGMP-dependent protein kinase G (PKG) implicated as a protective mechanism against ischemic injury in diverse animal models from insects mammals. In Drosophila, increased PKG results survival animals exposed stress. To determine if the NO/cGMP/PKG pathway is at level, present study employed pharmacological protocol mimic hypoxic S2 cells. commonly cell line was derived primary culture late stage (20–24 h old) melanogaster embryos. Hypoxic induced by exposure either sodium azide (NaN3) or cobalt chloride (CoCl2). During chemical stress, protected death this involved modulation mitochondrial ATP-sensitive potassium ion channels (mitoKATP). protection afforded during ischemia-like may be adaptive cytoprotective cascade could serve potential therapeutic target hypoxia ischemia-induced injury.