Propofol induces mitochondrial-associated protein LRPPRC and protects mitochondria against hypoxia in cardiac cells.

ABSTRACT:

Background

Hypoxia-induced oxidative stress is one of the main mechanisms of myocardial injury, which frequently results in cardiomyocyte death and precipitates life-threatening heart failure. Propofol (2,6-diisopropylphenol), which is used to sedate patients during surgery, was shown to strongly affect the regulation of physiological processes, including hypoxia-induced oxidative stress. However, the exact mechanism is still unclear.

Methods

Expression of LRPPRC, SLIRP, and Bcl-2 after propofol treatment was measured by RT-qPCR and western blot analyses. The effects of propofol under hypoxia were determine by assessing mitochondrial homeostasis and mitochondrial function, including the ATP level and mitochondrial mass. Autophagy/mitophagy was measured by detecting the prese

SUBMITTER: Zhang Q 

PROVIDER: S-EPMC7478836 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature