<p>Metabolic Dysfunction-Associated Fatty Liver Disease (MAFLD) is one of the most prevalent liver disorders worldwide, yet effective treatment options remain limited. The imbalance between hepatic lipid synthesis and oxidation serves as its primary pathogenic mechanism. The SREBP-1c/FAS/ACCα pathway and PPARα/CPT-1 pathway, acting as key regulators of lipid synthesis and oxidative degradation respectively, play pivotal roles in the development of MAFLD. In this study, we demonstrated that <i>Chrysanthemum morifolium</i> (CM) ameliorates liver injury induced by lipid deposition in MAFLD mice, including attenuated steatosis, effective clearance of serum Triglyceride (TG), Total Cholesterol (TC), and low-density lipoprotein (LDL-C), as well as elevated high-density lipoprotein (HDL-C) levels. Further studies showed that among the monomeric compounds isolated from CM lignocellulosic acid (LU), hexaconitine (AR), and lignocellulosic acid-7-O-β-D-glucopyranoside (LU-glu) reduced the lipotropic activity through the SREBP-1c/FAS/ACCα and PPARα/CPT-1 pathways. Overall, our results demonstrate that CM alleviates MAFLD symptoms by inhibiting the SREBP-1c/FAS/ACCα pathway to reduce lipid synthesis while activating the PPARα/CPT-1 pathway to enhance oxidation, thereby maintaining hepatic metabolic homeostasis. This provides a new direction for the development and application of drugs to treat MAFLD.</p>

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Chrysanthemum morifolium extract improves metabolic dysfunction-associated fatty liver disease by regulating lipid metabolism

  • Wenjing Yu,
  • Jun Qiu,
  • Yonghu Chen,
  • Xianhua Che,
  • Xuezheng Li

摘要

Metabolic Dysfunction-Associated Fatty Liver Disease (MAFLD) is one of the most prevalent liver disorders worldwide, yet effective treatment options remain limited. The imbalance between hepatic lipid synthesis and oxidation serves as its primary pathogenic mechanism. The SREBP-1c/FAS/ACCα pathway and PPARα/CPT-1 pathway, acting as key regulators of lipid synthesis and oxidative degradation respectively, play pivotal roles in the development of MAFLD. In this study, we demonstrated that Chrysanthemum morifolium (CM) ameliorates liver injury induced by lipid deposition in MAFLD mice, including attenuated steatosis, effective clearance of serum Triglyceride (TG), Total Cholesterol (TC), and low-density lipoprotein (LDL-C), as well as elevated high-density lipoprotein (HDL-C) levels. Further studies showed that among the monomeric compounds isolated from CM lignocellulosic acid (LU), hexaconitine (AR), and lignocellulosic acid-7-O-β-D-glucopyranoside (LU-glu) reduced the lipotropic activity through the SREBP-1c/FAS/ACCα and PPARα/CPT-1 pathways. Overall, our results demonstrate that CM alleviates MAFLD symptoms by inhibiting the SREBP-1c/FAS/ACCα pathway to reduce lipid synthesis while activating the PPARα/CPT-1 pathway to enhance oxidation, thereby maintaining hepatic metabolic homeostasis. This provides a new direction for the development and application of drugs to treat MAFLD.