Your browser doesn't support javascript.
loading
Botanical Antcin K Alleviates High-Fat Damage in Palm Acid Oil-Treated Vascular Endothelial Cells and Macrophages.
Lu, Chen-Wen; Nguyen, Ngan Thi Kim; Shen, Szu-Chuan; Wu, Yeh-Bin; Liang, Hui-Ju; Wu, Chung-Hsin.
  • Lu CW; School of Life Science, National Taiwan Normal University, Taipei 11677, Taiwan.
  • Nguyen NTK; School of Life Science, National Taiwan Normal University, Taipei 11677, Taiwan.
  • Shen SC; School of Life Science, National Taiwan Normal University, Taipei 11677, Taiwan.
  • Wu YB; ARJIL Pharmaceuticals LLC, Hsinchu City 30013, Taiwan.
  • Liang HJ; ARJIL Pharmaceuticals LLC, Hsinchu City 30013, Taiwan.
  • Wu CH; School of Life Science, National Taiwan Normal University, Taipei 11677, Taiwan.
Plants (Basel) ; 11(21)2022 Oct 22.
Article en En | MEDLINE | ID: mdl-36365265
ABSTRACT
Lipid metabolism disorder is the most critical risk factor for atherosclerosis, and the process involves lipid deposition in the arterial intima. In Taiwan, antcin K, an active triterpenoid from the fruiting bodies of Antrodia camphorata, has been considered a potential lipid-lowering agent. Despite this, the possible therapeutic mechanisms of antcin K remain unclear. To explore the crucial role of botanical antcin K in reducing atherosclerotic plaque, we used SVEC4-10 vascular endothelial cells and RAW264.7 macrophages with palm acid oil-induced high-fat damage as our cell models. Our results showed through using the DPPH assay that antcin K had excellent free radical scavenging ability. Antcin K treatment can significantly alleviate the high-fat damage and reduce the levels of inflammatory factors of TNF-α and IL-1ß in vascular endothelial cells and macrophages, as shown through MTT assay and ELISA. Furthermore, antcin K treatment can effectively enhance migration ability and clear lipid deposition in macrophages, as shown by using cell migration assay and oil red O staining. When stained with immunofluorescence, antcin K was shown to significantly decrease the expression of adhesion molecules of vascular cell adhesion molecule 1 (VCAM-1) in vascular endothelial cells involved in monocyte migration and inflammation. Antcin K not only reduced the expression of the CD36 scavenger receptor but also augmented the expression of Kruppel-like factor 4 (KLF4) transcription factor in macrophages, which inhibits the transformation of macrophages into foam cells underlying the pathological process of atherosclerosis. Taking our findings into account, we suggested that botanical antcin K could have therapeutic potential for the treatment of atherosclerosis.
Palabras clave

Texto completo: 1 Banco de datos: MEDLINE Tipo de estudio: Prognostic_studies / Risk_factors_studies Idioma: En Año: 2022 Tipo del documento: Article

Texto completo: 1 Banco de datos: MEDLINE Tipo de estudio: Prognostic_studies / Risk_factors_studies Idioma: En Año: 2022 Tipo del documento: Article