Dimethylcurcumin Alleviates Copper Sulfate-Induced Toxicity by Regulating Glycolipid Metabolism and Arachidonic Acid Metabolism.

The present study aimed to evaluate the effects of dimethylcurcumin (DMC) on copper sulfate (CuSO4)-induced inflammatory toxicity in zebrafish, and preliminarily explore its potential molecular mechanism. Zebrafish larvae at 3 days post-fertilization (3 dpf) were pretreated with different concentrations of DMC for 24 h, followed by a 2 h exposure to CuSO4. Inflammatory cell migration and aggregation, reactive oxygen species (ROS) levels, and locomotor activity were then determined to evaluate the protective effect of DMC against CuSO4-induced toxicity. To investigate the potential mechanisms through which DMC confers protection against CuSO4-induced toxicity, RT-qPCR verification and molecular docking analyses were conducted. Compared with the control group, CuSO4-treated zebrafish exhibited aggravated inflammatory cell migration, elevated ROS levels, and reduced locomotor distance and speed. However, DMC pretreatment markedly alleviated inflammatory cell migration and restored locomotor activity compared with the CuSO4-treated group. Transcriptomic analysis revealed that differentially expressed genes were mainly enriched in metabolic pathways, including starch and sucrose metabolism, steroid hormone biosynthesis and arachidonic acid metabolism. RT-qPCR and molecular docking analyses further substantiated changes in the expression of relevant genes involved in these pathways. DMC has the potential to alleviate CuSO4-induced toxicity in zebrafish. Its protective mechanism may be associated with the modulation of glycolipid and arachidonic acid metabolism.