Protective Effect of Oxytocin Against Apoptosis and Oxidative Stress: Role of Extracellular Signal Regulating Kinases

Abstract

Neuropeptide oxytocin plays a role in the neuronal proliferation, differentiation and affects related morphological changes of neuronal cells. It has been suggested that oxytocin has protective effect against inflammation and consequences of oxidative stress. However, mechanisms of its action at the molecular level are not fully understood. The aim of the present study was to determine oxytocin anti‐apoptotic effects and potential inhibition of oxidative stress in glioblastoma U87‐MG cell line. We have clearly shown that activation of oxytocin receptors dose‐dependently stimulated proliferation of U‐87MG cells. Incubation of cells in the presence of oxytocin increased ERK1/2 phosphorylation, which was reduced by oxytocin receptor antagonist. Our results also revealed that in the U87‐MG cell‐line, hydrogen peroxide (H2O2) increased the intracellular reactive oxygen species (ROS) production in a dose‐dependent manner. Interestingly, cells treated with H2O2 in the presence of oxytocin showed a significant decline in the ROS production. We have also confirmed that oxytocin mediates its protective effect in U87‐MG cells through activation of the MAPK/ERK ½ signaling pathway. The protective effect of oxytocin has been observed against consequences of oxidative stress in peroxide model and apoptosis induced by camptothecin, as well. To our best knowledge this is the first study demonstrating that there is interference in production of ROS and activation of oxytocin receptors in neuronal cells. Overall, the present data indicate that oxytocin stimulates proliferation and protects glial cells against apoptosis and oxidative stress.Support or Funding Information1‐ President's Faculty Research & Development (PFRDG) Grant ‐ 2015–20162‐ Saudi Arabian Cultural Mission (SACM) Graduate Students Research GrantThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.