Morin, a matrix metalloproteinase 9 inhibitor, attenuates endothelial-to-mesenchymal transition in atherosclerosis by downregulating Notch-1 signaling

J Integr Med. 2024 Nov;22(6):683-695. doi: 10.1016/j.joim.2024.11.002. Epub 2024 Nov 8.

Abstract

Objective: Atherosclerotic cardiovascular disease poses a significant health challenge globally. Recent findings highlight the pivotal role of the endothelial-to-mesenchymal transition (EndMT) in atherosclerosis. Morin is a bioflavonoid mainly extracted from white mulberry, a traditional Chinese herbal medicine with anti-inflammatory and antioxidant properties. This study examines whether morin can alleviate atherosclerosis by suppressing EndMT and seeks to elucidate the underlying mechanism.

Methods: We induced an in vitro EndMT model in human umbilical vein endothelial cells (HUVECs) by stimulating the cells with transforming growth factor-β1 (TGF-β1) (10 ng/mL) for 48 h. The in vivo experiments were performed in an atherosclerosis model using apolipoprotein E (ApoE)-/- mice fed with a high-fat diet (HFD). Mice in the intervention group were given morin (50 mg/kg) orally for 4 weeks. Molecular docking and microscale thermophoresis were assayed to understand the interactions between morin and matrix metalloproteinase-9 (MMP-9).

Results: Morin inhibited the expression of EndMT markers in a dose-dependent manner in TGF-β1-treated HUVECs. Administering 50 μmol/L morin suppressed the upregulation of MMP-9 and Notch-1 signaling in TGF-β1-induced EndMT. Moreover, the overexpression of MMP-9 activated Notch-1 signaling, thereby reversing morin's inhibitory effect on EndMT. In the HFD-induced atherosclerotic ApoE-/- mice, morin notably reduced aortic intimal hyperplasia and plaque formation by suppressing EndMT. Furthermore, morin demonstrated a strong binding affinity for MMP-9.

Conclusion: Morin acts as an MMP-9 inhibitor to disrupt EndMT in atherosclerosis by limiting the activation of Notch-1 signaling. This study underscores morin's potential utility in the development of anti-atherosclerotic medication. Please cite this article as: He Y, Qin XX, Liu MW, Sun W. Morin, a matrix metalloproteinase 9 inhibitor, attenuates endothelial-to-mesenchymal transition in atherosclerosis by downregulating Notch-1 Signaling. J Integr Med. 2024; 22(6): 684-696.

Keywords: Atherosclerosis; Endothelial-to-mesenchymal transition; Matrix metalloproteinase-9; Morin; Traditional Chinese medicine.

MeSH terms

  • Animals
  • Atherosclerosis* / drug therapy
  • Atherosclerosis* / metabolism
  • Down-Regulation* / drug effects
  • Epithelial-Mesenchymal Transition* / drug effects
  • Flavones
  • Flavonoids* / pharmacology
  • Human Umbilical Vein Endothelial Cells* / drug effects
  • Humans
  • Male
  • Matrix Metalloproteinase 9* / genetics
  • Matrix Metalloproteinase 9* / metabolism
  • Matrix Metalloproteinase Inhibitors / pharmacology
  • Mice
  • Mice, Inbred C57BL
  • Receptor, Notch1* / genetics
  • Receptor, Notch1* / metabolism
  • Signal Transduction* / drug effects
  • Transforming Growth Factor beta1 / genetics
  • Transforming Growth Factor beta1 / metabolism

Substances

  • Flavonoids
  • morin
  • Receptor, Notch1
  • Matrix Metalloproteinase 9
  • Transforming Growth Factor beta1
  • Matrix Metalloproteinase Inhibitors
  • Flavones