4.7 Article

Mulberry Leaf and Neochlorogenic Acid Alleviates Glucolipotoxicity-Induced Oxidative Stress and Inhibits Proliferation/Migration via Downregulating Ras and FAK Signaling Pathway in Vascular Smooth Muscle Cell

Journal

NUTRIENTS
Volume 14, Issue 15, Pages -

Publisher

MDPI
DOI: 10.3390/nu14153006

Keywords

neochlorogenic acid; diabetic atherosclerosis; FAK signals; mulberry leaf extract; VSMC migration and proliferation

Funding

  1. Chung Shan Medical University Hospital, Taichung, Taiwan [CSH-2019-C-022, CSH-2021-C-034]
  2. Taiwan Ministry of Science and Technology [110-2320-B-040-010]

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The study found that mulberry leaf extract and neochlorogenic acid can inhibit the proliferation and migration of rat aortic vascular smooth muscle cells under diabetic conditions. These effects may be achieved through the inhibition of FAK/small GTPase proteins, PI3K/Akt, and Ras-related signaling.
Mulberry leaf (Morus alba L.) has been used as a health food and in traditional medicine to treat several metabolic diseases, including diabetes, hypertension, and hyperlipidemia. However, the mechanism by which mulberry leaf and its functional components mediate atherosclerosis remains unclear. This study aimed to determine the effect of mulberry leaf extract (MLE) and its major component, neochlorogenic acid (nCGA), on the proliferation and migration of rat aortic vascular smooth muscle cells (VSMCs, A7r5 cell line) under diabetic cultured conditions (oleic acid and high glucose, OH). Our findings showed that MLE and nCGA significantly inhibited cell proliferation and migration in A7r5 cells as determined by a scratch wound assay and a Transwell assay. Furthermore, we observed MLE and nCGA inhibited cell proliferation and migration, such as reducing the phosphoinositide 3-kinases (PI3K)/protein kinase B (Akt), focal adhesion kinase (FAK), and small GTPase proteins using Western blot analysis. In conclusion, we confirmed the anti-atherosclerotic effects of MLE and nCGA in reducing vascular smooth muscle cell (VSMC) migration and proliferation under diabetic cultured conditions via inhibition of FAK/small GTPase proteins, PI3K/Akt, and Ras-related signaling.

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