TDCPP protects cardiomyocytes from H₂O₂-induced injuries via activating PI3K/Akt/GSK3β signaling pathway.

Tris (1, 3-dichloro-2-propyl) phosphate (TDCPP) is a major type of organophosphorus flame retardants, and long-term exposure to TDCPP to normal cells or tissues under physiological conditions can induce toxic effects. But how TDCPP leads to the adverse effects is not yet clear, and the effect of TDCPP under pathological conditions such as reactive oxygen species assault is not well understood. The present study aimed to explore the potential effect of TDCPP against H₂O₂-induced oxidative stress in H9c2 cardiomyoblasts and rat neonatal cardiomyocytes. We found that H₂O₂-treatment decreased cell viability and increased lactate dehydrogenase and malondialdehyde generation of H9c2 cells. However, TDCPP could alleviate these effects. TDCPP alleviated Ca²⁺-overload caused by H₂O₂ through decreasing store-operated calcium entry. More importantly, TDCPP remarkably decreased H₂O₂-induced dephosphorylation of Akt and GSK3β, and through this pathway TDCPP mitigated the H₂O₂-induced apoptosis and detrimental autophagy. Collectively, via mitigating Ca²⁺-overload and activating the Akt/GSK3β signaling pathway, TDCPP may have a role in protecting cardiomyocytes from oxidative stress.

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