Dibutyl phthalate-induced oxidative stress, inflammation and apoptosis in grass carp hepatocytes and the therapeutic use of taxifolin

Abstract

The widespread use of plastic products has led to the widespread presence of plasticizers in the environment. As a common environmental pollutant, research on plasticizer toxicity is insufficient in fish cells. In particular, research on the toxicity of dibutyl phthalate (DBP) in grass carp hepatocyte lines is insufficient. To further explore these mechanisms, we treated grass carp hepatocytes with 300 μM DBP, a common plasticizer, for 24 h, and hepatocytes were also treated with 1 μM taxifolin (TAX), an antioxidant, for 24 h to study its antagonistic effect on DBP. After DBP exposure, oxidative stress levels and inflammation in hepatocytes increased, and the mRNA and protein expression of apoptosis-related markers increased significantly, leading to hepatocyte apoptosis. Moreover, AO/EB staining, Hoechst staining and flow cytometry also showed that the level of apoptotic cells increased after DBP exposure. Notably, both TAX pretreatment and TAX simultaneous treatment alleviated oxidative stress, increased inflammatory factor levels and apoptosis induced by DBP. In comparison, the effect of simultaneous TAX treatment was better than that of TAX pretreatment. Our results showed that TAX alleviates DBP-induced apoptosis in grass carp hepatocytes through oxidative stress and inflammation, and TAX pretreatment and simultaneous treatment exhibited specific effects. Specifically, simultaneous treatment had a better effect. Our study assessed the toxicity of DBP in grass carp hepatocytes and provided a theoretical and research basis for the in vivo study of animal models in the future. The innovation of this study involves the exploration of the interaction between DBP and TAX for the first time. This study may enrich knowledge regarding the theoretical mechanism of DBP toxicity in fish hepatocytes and propose methods address DBP toxicity.