Transcriptome Sequencing Reveals That Curcumin Protects Leghorn Chicken Cardiomyocytes from Heat Stress-Induced Iron Dysregulation.

The purpose of this study was to offer a theoretical foundation for the use of curcumin in poultry systems for anti-stress responses. Fourteen-day-old SPF Leghorn embryonic eggs were isolated and digested to produce primary cultured cardiomyocytes for this investigation. The primary cultured cardiomyocytes were divided into three groups: the CK group, serving as the control check; the HS group, which underwent a heat stress challenge; and the HS_Cur group, which was pre-treated with curcumin prior to experiencing heat stress. Twenty hours prior to the heat stress phase, the HS_Cur group received 15 μmol/L of curcumin. The culture medium's cells and supernatant were extracted. Curcumin has been shown to protect cells against heat stress by drastically inhibiting the release of CK-MB and LDH, reducing the generation of MDA, and improving the potential of the mitochondrial membrane. Heat stress may alter cell proliferation, the base repair process, and cause proteotoxic stress, according to pathway enrichment analysis. Several iron metabolism-related pathways were both shown in CK vs. HS and HS vs. HS_Cur comparisons. Curcumin can promote heme synthesis and improve iron storage and antioxidant capacity by suppressing the expression of FTL, MAP1LC3C, and FXN and increasing the expression of SLC7A11, FTH1, FECH, SQSTM1, and NQO1, according to our subsequent analysis of iron metabolism-related DEGs. Curcumin may protect cells from the toxicity of LIP by inhibiting the expression of ferritinophagy-related genes and increasing the expression of heme production, iron storage, and antioxidant-related genes.