Chan Kuei-Chuan, Ho Hsieh-Hsun, Lin Ming-Cheng, Huang Chien-Ning, Huang Hui-Pei, Wang Chau-Jong
Department of Internal Medicine, Chung Shan Medical University Hospital, No. 110, Sec. 1, Jianguo N. Road, Taichung 402, Taiwan.
School of Medicine, Institute of Medicine, Chung Shan Medical University, No. 110, Sec. 1, Jianguo N. Road, Taichung 402, Taiwan.
J Sci Food Agric. 2016 Jan 30;96(2):381-91. doi: 10.1002/jsfa.7100. Epub 2015 Feb 19.
Previous studies have shown that mulberry polyphenolic compounds have an anti-atherosclerotic effect in rabbits. Apoptosis of vascular smooth muscle cells (VSMCs) is the key determinant of the number of VSMCs in remodeling. To examine the effect of mulberry polyphenol extracts (MPEs) on the apoptosis of VSMCs and thus the prevention of atherosclerosis, this study investigated the ability of MPEs to induce apoptosis in vitro and the underlying mechanism.
It was found that MPEs initially activated JNK/p38 and p53, which in turn activated both Fas-ligand and mitochondrial pathways, thereby causing mitochondrial translocation of Bax and a reduction in Bcl-2. This then triggered the cleavage of procaspases, finally resulting in apoptosis of VSMCs.
This study shows that MPEs may suppress atherosclerosis through stimulating apoptosis of VSMCs via activating JNK/p38 and p53 signaling.
先前的研究表明,桑椹多酚化合物对家兔具有抗动脉粥样硬化作用。血管平滑肌细胞(VSMC)凋亡是重塑过程中VSMC数量的关键决定因素。为了研究桑椹多酚提取物(MPE)对VSMC凋亡的影响以及对动脉粥样硬化的预防作用,本研究调查了MPE在体外诱导凋亡的能力及其潜在机制。
发现MPE最初激活JNK/p38和p53,进而激活Fas配体和线粒体途径,从而导致Bax向线粒体转位并使Bcl-2减少。随后引发前半胱天冬酶的裂解,最终导致VSMC凋亡。
本研究表明,MPE可能通过激活JNK/p38和p53信号通路刺激VSMC凋亡来抑制动脉粥样硬化。