The Extract of Camellia Seed Cake Alleviates Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) in Mice by Promoting Coenzyme Q Synthesis

<b>Background</b>: Metabolic dysfunction-associated steatotic liver disease (MASLD) is a prevalent metabolic disorder. Camellia seed cake, a byproduct of oil extraction, contains a variety of bioactive compounds. This study investigated the regulatory effects and underlying mechanisms of camellia seed cake extract (CSCE) using a high-fat diet (HFD)-induced MASLD mouse model. <b>Methods</b>: Mice were divided into four groups: normal control (N, standard diet), HFD model (M), HFD-fed mice treated with low-dose CSCE (L), and HFD-fed mice treated with high-dose CSCE (H). CSCE was administered via oral gavage for eight weeks. Body weight, blood lipid levels, liver weight, hepatic lipid accumulation, oxidative stress markers, ATP levels, and the NADH/NAD⁺ ratio were measured. Transcriptomic and lipidomic analyses were performed to identify potential regulatory pathways, and qPCR analysis was conducted to confirm the expression levels of essential genes. <b>Results</b>: CSCE significantly reduced HFD-induced increases in body and liver weights, improved blood lipid profiles and hepatic lipid accumulation, alleviated oxidative stress, increased ATP levels, and reduced the NADH/NAD⁺ ratio. Transcriptomic analysis demonstrated notable enrichment of genes associated with oxidative phosphorylation, mitochondrial function, and lipid metabolism after treatment. The lipidomic analysis demonstrated that the hepatic lipid profile of the H group approached that of the N group, with Coenzyme Q9 (CoQ9) and Coenzyme Q10 (CoQ10) levels significantly increased by 173.32% and 202.73%, respectively, compared to the M group. qPCR validation confirmed that CoQ synthesis-related genes (<i>Coq2-10</i>, <i>Pdss1</i>, <i>Pdss2</i>, and <i>Hmgcr</i>) were significantly upregulated in the treatment groups. <b>Conclusions</b>: CSCE enhances mitochondrial function by promoting CoQ synthesis, alleviates metabolic dysfunction, and could represent a potential natural intervention for MASLD.