Polysaccharide from Fuzi protects against Ox‑LDL‑induced calcification of human vascular smooth muscle cells by increasing autophagic activity.
Polysaccharide from Fuzi protects against Ox‑LDL‑induced calcification of human vascular smooth muscle cells by increasing autophagic activity.
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附子多糖通过增加自噬活性来防止 Ox-LDL 诱导的人血管平滑肌细胞钙化
DOI：
10.3892/mmr.2018.8488
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发表时间：
2018-04
影响因子：
3.4
通讯作者：
Liu Y
中科院分区：
文献类型：
--
作者：
Liao L;Zhuang X;Li W;Su Q;Zhao J;Liu Y
附子多糖（FPS）是从传统中草药附子中分离得到的一种水溶性多糖。已被证明可以通过其有效的抗氧化作用保护肝细胞免受缺血再灌注损伤，并通过增加自噬活性来减弱饥饿诱导的H9 c2细胞细胞毒性。采用茜素红S染色法检测心肌矿物质沉积，逆转录-定量聚合酶链反应（RT-PCR）检测心肌核心结合因子α1和平滑肌22α mRNA表达。为分析自噬活性，使用蛋白质印迹法检测微管相关蛋白1A/1B轻链3和核孔蛋白P62的表达。此外，通过荧光显微镜观察到每个细胞中有绿色荧光蛋白-LC 3点。氧化型低密度脂蛋白（Ox-LDL）可浓度依赖性地促进人血管平滑肌细胞（VSMCs）钙化，FPS对Ox-LDL诱导的VSMCs钙化有明显的保护作用。此外，FPS治疗减轻了Ox-LDL诱导的自噬活性的下调，FPS对Ox-LDL诱导的钙化的保护作用被自噬抑制剂3-甲基腺嘌呤减弱。总之，本研究首次证明了作者所知的FPS可以保护人VSMCs免受Ox-LDL诱导的血管钙化，并且这可能通过激活自噬发生。这支持了自噬可能是抵抗血管钙化的内源性保护机制的假设，并且FPS可用作血管钙化的潜在治疗剂。
Polysaccharide from Fuzi (FPS) is a water-soluble polysaccharide isolated from the traditional Chinese herbal medicine Fuzi. It has been demonstrated to protect hepatocytes against ischemia-reperfusion injury through its potent antioxidant effects, and to attenuate starvation-induced cytotoxicity in H9c2 cells by increasing autophagic activity. In the present study, Alizarin Red S staining was used to detect mineral deposition and reverse transcription-quantitative polymerase chain reaction was used to detect the core binding factor α1 and smooth muscle 22α mRNA expression. To analyze autophagic activity, western blotting was used to detect microtubule-associated protein 1A/1B light chain 3 and nucleoporin P62 expression. In addition, green fluorescent protein-LC3 dots-per-cell was observed by fluorescence microscopy. It was demonstrated that oxidized low-density lipoprotein (Ox-LDL) could increase the calcification of human vascular smooth muscle cells (VSMCs) in a concentration-dependent manner, and that FPS treatment had a significant protective effect against Ox-LDL-induced calcification of human VSMCs. Furthermore, FPS treatment alleviated the Ox-LDL-induced downregulation of autophagic activity, and the protective effect of FPS on Ox-LDL-induced calcification was attenuated by the autophagy inhibitor 3-methyladenine. In conclusion, the present study demonstrated for the first time to the best of the authors' knowledge that FPS can protect against Ox-LDL-induced vascular calcification in human VSMCs, and that this likely occurs via the activation of autophagy. This supports the hypothesis that autophagy may be an endogenous protective mechanism counteracting vascular calcification, and that FPS may be used as a potential therapeutic for vascular calcification.
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影响因子：
9.3
作者：
Leopold JA
通讯作者：
Leopold JA
附子多糖可能通过激活 AMPK/mTOR 通路来增加自噬，从而防止 H9c2 细胞中饥饿诱导的细胞毒性
影响因子：
5.7
作者：
Liao, Li-Zhen;Chen, Yan-Ling;Wu, Wei-Kang
通讯作者：
Wu, Wei-Kang
影响因子：
37.8
作者：
Bild, DE;Detrano, R;Saad, MF
通讯作者：
Saad, MF
影响因子：
5.3
作者：
Han, Xue;Wang, Li-Yan;Liu, Wen-Hu
通讯作者：
Liu, Wen-Hu
影响因子：
4
作者：
Liu, Hongmei;Lu, Qian;Huang, Kaixun
通讯作者：
Huang, Kaixun