Department of Pharmacy, the First Affiliated Hospital of Anhui University of Chinese Medicine, Hefei 230031, China.
School of Integrated Traditional and Western Medicine, Anhui University of Chinese Medicine, Hefei 230012, China.
J Tradit Chin Med. 2024 Feb;44(1):103-112. doi: 10.19852/j.cnki.jtcm.20231215.003.
To investigate the effect of Taohong Siwu decoction (, TSD) on atherosclerosis in rats as well as investigate the underlying mechanism based on molecular docking.
Sixty healthy male Sprague-Dawley rats were randomly divided into 6 groups with 10 rats in each group: control group, model group, atorvastatin group (AT, 2.0 mg/kg), and TSD groups (20, 10, 5 g/kg) after 7 d of acclimation. The model of atherosclerosis was successfully established except the control group by high fat diet (HFD) and vitamin D. Biochemical analyzers were used to detect the levels of triglyceride (TG), total cholestero (TC), low density lipoprotein-cholesterol (LDL-C) and high density lipid-cholesterol (HDL-C) in blood lipid. The levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and interleukin-1β (IL-1β) were determined by enzyme-linked immunosorbent assay. Sudan IV staining and Hematoxylin and eosin staining (HE staining) were performed to observe the pathological changes in aortic tissue. Molecular docking technology was used to predict the best matching between the main components of TSD and the target proteins. The expression of target proteins was further detected by quantitative real time polymerase chain reaction (qRT-PCR) and Western blot analysis.
The results showed that TSD restricted atherosclerosis development and decreased the inflammatory cytokines in plasma. Molecular docking results predicted that the main components of TSD showed a strong binding ability with toll-like receptor (TLR4), myeloid differentiation primary response protein 88 (MyD88), and nuclear factor kappa-B (NF-κB). The results of qRT-PCR and Western blot analysis showed that the mRNA and protein expressions of TLR4, MyD88 and NF-κB p65 in the aorta were reduced in atorvastatin group and TSD group.
TSD can ameliorate atherosclerosis in rats, and the underlying mechanism is supposed be related to the suppression of inflammatory response by regulating TLR4/MyD88/NF-κB signal pathway.
探讨桃红四物汤（TSD）对大鼠动脉粥样硬化的影响，并基于分子对接研究其作用机制。
60 只健康雄性 Sprague-Dawley 大鼠随机分为 6 组，每组 10 只：除对照组外，其余 5 组大鼠均给予高脂饲料（HFD）和维生素 D 喂养 7 d 以建立动脉粥样硬化模型。采用生化分析仪检测各组大鼠血清中甘油三酯（TG）、总胆固醇（TC）、低密度脂蛋白胆固醇（LDL-C）和高密度脂蛋白胆固醇（HDL-C）水平，酶联免疫吸附试验检测肿瘤坏死因子-α（TNF-α）、白细胞介素-6（IL-6）和白细胞介素-1β（IL-1β）水平，苏丹 IV 染色和苏木精-伊红（HE）染色观察主动脉组织病理变化，分子对接技术预测 TSD 主要成分与靶蛋白的最佳匹配，并进一步通过定量实时聚合酶链反应（qRT-PCR）和 Western blot 分析检测靶蛋白的表达。
结果表明，TSD 可抑制动脉粥样硬化发展，降低血浆中炎症因子水平。分子对接结果预测 TSD 的主要成分与 toll 样受体（TLR4）、髓样分化初级反应蛋白 88（MyD88）和核因子 kappa-B（NF-κB）具有较强的结合能力。qRT-PCR 和 Western blot 分析结果显示，阿托伐他汀组和 TSD 组大鼠主动脉 TLR4、MyD88 和 NF-κB p65 的 mRNA 和蛋白表达均降低。
TSD 可改善大鼠动脉粥样硬化，其作用机制可能与通过调节 TLR4/MyD88/NF-κB 信号通路抑制炎症反应有关。
