Perfluorooctanesulfonic acid (PFOS), a fluorine-containing
organic
compound, can be widely detected in the environment and living organisms.
Accumulating evidence has shown that PFOS breaks through different
biological barriers resulting in cardiac toxicity, but the underlying
molecular mechanisms remain unclear. Cannabidiol (CBD) is a nonpsychoactive
cannabinoid without potential adverse cardiotoxicity and has antioxidant
and anti-inflammatory properties that reduce multiorgan damage and
dysfunction. For these reasons, the aim of this study was to research
how PFOS caused heart injury and whether CBD could attenuate PFOS-induced
heart injury. Mice were fed PFOS (5 mg/kg) and/or CBD (10 mg/kg) in
vivo. In vitro, H9C2 cells were intervened with PFOS (200 μM)
and/or CBD (10 μM). After PFOS exposure, oxidative stress levels
and the mRNA and protein expression of apoptosis-related markers increased
distinctly, accompanied by mitochondrial dynamic imbalance and energy
metabolism disorders in mouse heart and H9C2 cells. Moreover, terminal
deoxynucleotidyl transferase dUTP nick end labeling staining, acridine
orange/ethidium bromide staining and Hoechst 33258 staining signaled
that the number of apoptotic cells increased after exposure to PFOS.
Noteworthy, CBD simultaneous treatment alleviated a series of damages
caused by PFOS-mediated oxidative stress. Our results demonstrated
that CBD could alleviate PFOS-induced mitochondrial dynamics imbalance
and energy metabolism disorder causing cardiomyocyte apoptosis by
improving the antioxidant capacity, suggesting that CBD may represent
a novel cardioprotective strategy against PFOS-induced cardiotoxicity.
Our findings facilitate the understanding of the cardiotoxic effects
of PFOS and the important role of CBD in protecting cardiac health.