Diclofenac induces proteasome and mitochondrial dysfunction in murine cardiomyocytes and hearts.

ABSTRACT:

Background

One of the most common nonsteroidal anti-inflammatory drugs (NSAIDs) used worldwide, diclofenac (DIC), has been linked to increased risk of cardiovascular disease (CVD). The molecular mechanism(s) by which DIC causes CVD is unknown.

Methods

Proteasome activities were studied in hearts, livers, and kidneys from male Swiss Webster mice treated with either 100mg/kg DIC for 18h (acute treatment) or 10mg/kg DIC for 28days (chronic treatment). Cultured H9c2 cells and neonatal cardiomyocytes were also treated with different concentrations of DIC and proteasome function, cell death and ROS generation studied. Isolated mouse heart mitochondria were utilized to determine the effect of DIC on various electron transport chain complex activities.

Results

DIC significant

SUBMITTER: Ghosh R 

PROVIDER: S-EPMC5076377 | biostudies-literature | 2016 Nov

REPOSITORIES: biostudies-literature