Black goji berry (Lycium ruthenicum Murr.) is well-known for its high nutritional and medicinal value, largely due to its rich content of naturally occurring anthocyanins, which exhibit various health-promoting bioactivities. In this study, we established a paraquat-induced oxidative stress model in Caenorhabditis elegans and found that black goji berry anthocyanins (BGA) significantly extended lifespan and improved mobility. Additionally, BGA significantly increased catalase (CAT) activity and the GSH/GSSG ratio, while reducing oxidative damage markers, including ROS, malondialdehyde (MDA), and protein carbonyl levels, demonstrating potent anti-oxidative stress activity in vivo. Furthermore, BGA improved mitochondrial morphology, partially restored damaged mitochondrial membrane potential (MMP) and ATP levels, and elevated relative mitochondrial DNA level under oxidative stress. By analyzing pyruvate, lactate, and TCA cycle metabolites, we hypothesize that BGA may enhance energy metabolism, with its mitochondrial protective effects mainly attributed to its petunidin derivatives, particularly petunidin-3-O-glucoside. Gene expression analysis revealed that BGA upregulated key electron transport chain genes, including cco-1, atp-2, and clk-1, potentially enhancing energy metabolism. Further investigation of lifespan, ROS levels, and gene expression in clk-1 mutants confirmed the critical role of clk-1 in BGA-mediated mitochondrial protection and oxidative stress resistance. Our findings provide new insights into the molecular pathways through which BGA exerts its protective effects against oxidative stress in vivo, supporting the potential use of black goji berry and its anthocyanins as functional foods and nutrients with anti-oxidative stress and mitochondrial-protective properties.
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