Department of Cardiology, The First Affiliated Hospital of Xi'an Jiao Tong University, Xi'an City, Shaanxi Province, 710061, China.
Department of Cardiology, Han Zhong Central Hospital, Hanzhong City, Shaanxi Province, 723000, China.
Biomed Pharmacother. 2018 Jan;97:1673-1679. doi: 10.1016/j.biopha.2017.12.024. Epub 2017 Dec 8.
Atherosclerosis (AS) is a chronic progressive disease related to inflammatory reaction. Baicalin is a flavonoid isolated from Scutellaria baicalensis georgi (Huang-qin) and exerts anti-inflammation effects in various diseases. Here, we investigated the protective effects of baicalin treatment and the potential mechanism in AS progression on AS mouse model. After ApoE-/- mice with high-lipid diets had received 12 weeks' of baicalin treatment at different concentrations, plasma lipids levels and atherosclerotic plaque areas in aorta were measured and there exhibited a prominent improvement in the baicalin treated mice compared with mice in AS model group. The expression of lipolysis related proteins (PPARα, CPT-1) was increased while the expression of adipogenesis related proteins (SREBP-1c, ACS) was decreased by baicalin treatment, indicating the anti-adipogenic effect of baicalin. Moreover, baicalin up-regulated the activities of antioxidant enzymes (SOD, CAT and GSH-Px) and down-regulated the activity of oxidative parameter MDA compared with AS model group, indicating the anti-oxidant effect of baicalin. The increased levels of pro-inflammatory cytokines (IL-6, TNF-α, sVE-cadherin) induced by AS were also decreased by baicalin treatment, indicating that baicalin acted as an anti-inflammation regulator in AS. In addition, we further explored the potential mechanism of baicalin treatment on AS, and found that baicalin treatment attenuated the high phosphorylation levels of JNK, p65, p-38 and ERK1/2 induced by AS, indicating that baicalin treatment inhibited the NF-κB and p38 MAPK signaling pathways in AS. In conclusion, baicalin treatment inhibited the NF-κB and p38 MAPK signaling pathways, thereby achieved its anti-adipogenic effect, anti-oxidant effect and anti-inflammation effect in a dose-dependent manner in AS.
动脉粥样硬化（AS）是一种与炎症反应有关的慢性进行性疾病。黄芩苷是从黄芩（黄芩）中分离出来的一种黄酮类化合物，在各种疾病中具有抗炎作用。在这里，我们研究了黄芩苷治疗对 AS 进展的保护作用及其潜在机制。在 ApoE-/- 小鼠高脂饮食 12 周后，用不同浓度的黄芩苷进行治疗，测量血浆脂质水平和主动脉粥样硬化斑块面积，与 AS 模型组小鼠相比，黄芩苷治疗组小鼠有明显改善。黄芩苷处理增加了脂肪分解相关蛋白（PPARα、CPT-1）的表达，同时降低了脂肪生成相关蛋白（SREBP-1c、ACS）的表达，表明黄芩苷具有抗脂肪生成作用。此外，与 AS 模型组相比，黄芩苷上调了抗氧化酶（SOD、CAT 和 GSH-Px）的活性，下调了氧化参数 MDA 的活性，表明黄芩苷具有抗氧化作用。黄芩苷还降低了 AS 诱导的促炎细胞因子（IL-6、TNF-α、sVE-cadherin）的水平，表明黄芩苷在 AS 中起抗炎调节作用。此外，我们进一步探讨了黄芩苷治疗 AS 的潜在机制，发现黄芩苷治疗可减轻 AS 引起的 JNK、p65、p-38 和 ERK1/2 的高磷酸化水平，表明黄芩苷治疗抑制了 AS 中的 NF-κB 和 p38 MAPK 信号通路。总之，黄芩苷治疗通过抑制 NF-κB 和 p38 MAPK 信号通路，以剂量依赖的方式在 AS 中实现了其抗脂肪生成、抗氧化和抗炎作用。
