English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

We previously demonstrated the protective effect of hydrogen sulfide (H2S)against doxorubicin (DOX)-induced cardiotoxicity through inhibition of endoplasmicreticulum stress. The aim of the present study was to explore the role of p38mitogen-activated protein kinase (MAPK) in DOX-induced cardiotoxicity and ascertainwhether exogenous H2S protects DOX-induced injury by inhibiting p38 MAPK in cardiomyoblasts(H9c2). We observed that exposure of H9c2 cells to 5 µM DOX not only markedlyinduced injuries, including cytotoxicity, apoptosis, overproduction of reactiveoxygen species (ROS) and dissipation of mitochondrial membrane potential (MMP),but also enhanced the expression level of phosphorylated (p)-p38 MAPK. The DOX-inducedincrease in expression of p-p38 MAPK was significantly attenuated by pretreatmentof H9c2 cells with either 400 µM sodium hydrogen sulfide (NaHS) (a donor of H2S)or 1,000 µM N-acetyl-L-cysteine (NAC, an ROS scavenger) prior to exposure to DOX.Pretreatment with either 400 µM NaHS or 3 µM SB203580, a selective inhibitor ofp38 MAPK, ameliorated DOX-induced cardiomyocyte injuries, as evidenced by an increasein cell viability, and decreases in the number of apoptotic cells, ROS generationas well as dissipation of MMP. In conclusion, the findings of the present studydemonstrated that the activation of p38 MAPK contributes to DOX-induced injuries,including cytotoxicity, apoptosis, mitochondrial damage and oxidative stress inH9c2 cells. We also provide novel evidence that exogenous H2S protects H9c2 cellsagainst DOX-induced cardiotoxicity by inhibition of the p38 MAPK pathway.

Hydrogen sulfide attenuates doxorubicin-induced cardiotoxicity by inhibition of the p38 MAPK pathway in H9c2 cells