2. Academic Validation
  3. Morin hydrate inhibits atherosclerosis and LPS-induced endothelial cells inflammatory responses by modulating the NFκB signaling-mediated autophagy

Morin hydrate inhibits atherosclerosis and LPS-induced endothelial cells inflammatory responses by modulating the NFκB signaling-mediated autophagy

  • Int Immunopharmacol. 2021 Nov;100:108096. doi: 10.1016/j.intimp.2021.108096.
Qingyu Meng 1,  Luya Pu 1,  Qing Lu 2,  Baisen Wang 1,  Shuai Li 1,  Bin Liu 3,  Fan Li 4
Affiliations

Affiliations

  • 1 Department of Pathogenobiology, The Key Laboratory of Zoonosis, Chinese Ministry of Education, College of Basic Medicine, Jilin University, Changchun, China.
  • 2 Department of General Dentistry, School and Hospital of Stomatology, Jilin University, Changchun, Jilin, China.
  • 3 Cardiovascular Disease Center, The First Hospital of Jilin University, Changchun, China. Electronic address: [email protected].
  • 4 Department of Pathogenobiology, The Key Laboratory of Zoonosis, Chinese Ministry of Education, College of Basic Medicine, Jilin University, Changchun, China; Engineering Research Center for Medical Biomaterials of Jilin Province, Jilin University, Changchun, China; Key Laboratory for Health Biomedical Materials of Jilin Province, Jilin University, Changchun, China; State Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, Xinjiang, China; The Key Laboratory for Bionics Engineering, Ministry of Education, Jilin University, Changchun, China. Electronic address: [email protected].
PMID: 34464886 DOI: 10.1016/j.intimp.2021.108096
Abstract

Atherosclerosis (AS) is a chronic inflammatory disease involving blood vessels. Inflammation affects different cells and increases the expression of adhesion molecules. Morin hydrate (MO) is a naturally occurring bioflavonoid with anti-inflammatory and anti-oxidant effects. Although the exact mechanism has not been fully elucidated, MO possibly influences Autophagy pathways in immunity and inflammation. In this study, MO showed the potential to inhibit atherosclerotic and promote vascular endothelial Autophagy in apolipoprotein E (ApoE)-/- mice with a high-fat diet. Then, we aimed to explore the anti-inflammatory effects of MO in human umbilical vein endothelial cells (HUVECs) and its relationship with Autophagy. We found that MO inhibited lipopolysaccharide (LPS)-induced monocyte adhesion and the expression of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), cyclooxygenase-2 (COX-2), and matrix metallopeptidase 9 (MMP-9) in HUVECs. Moreover, MO reduced the expression of tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) by inhibiting the phosphatidylinositol-3-kinase (PI3K)/protein kinase B (Akt)/nuclear factor kappa B (NFκB) signaling pathway. MO induced Autophagy by inhibiting the NFκB signaling pathway in normal HUVECs and LPS-stimulated HUVECs. When Autophagy was inhibited by 3-methyladenine (3-MA) or small interfering RNA (siRNA), the anti-inflammatory effect of MO was reduced. In conclusion, MO inhibits atherosclerosis in ApoE-/- mice and LPS-induced inflammatory responses by inhibiting the activation of the PI3K/Akt1/NFκB signaling pathway in a NFκB signaling-mediated Autophagy way.

Keywords

Atherosclerosis; Autophagy; Inflammation; Morin hydrate; PI3K-Akt1-NFκB signaling pathway.

Figures
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    99.01%, Cell Proliferation Fluorescent Probe