Propofol inhibits parthanatos via ROS-ER-calcium-mitochondria signal pathway in vivo and vitro.

ABSTRACT: Parthanatos is a new form of programmed cell death. It has been recognized to be critical in cerebral ischemia-reperfusion injury, and reactive oxygen species (ROS) can induce parthanatos. Recent studies found that propofol, a widely used intravenous anesthetic agent, has an inhibitory effect on ROS and has neuroprotective in many neurological diseases. However, the functional roles and mechanisms of propofol in parthanatos remain unclear. Here, we discovered that the ROS-ER-calcium-mitochondria signal pathway mediated parthanatos and the significance of propofol in parthanatos. Next, we found that ROS overproduction would cause endoplasmic reticulum (ER) calcium release, leading to mitochondria depolarization with the loss of mitochondrial membrane potential. Mitochondria depolarization c

SUBMITTER: Zhong H 

PROVIDER: S-EPMC6141459 | biostudies-literature | 2018 Sep

REPOSITORIES: biostudies-literature