School of Traditional Chinese Medicine, Southern Medical University, Guangzhou 510515, China.
Integrated Hospital of Traditional Chinese Medicine, Southern Medical University, Guangzhou 510310, China.
J Tradit Chin Med. 2020 Dec;40(6):938-946. doi: 10.19852/j.cnki.jtcm.20200905.001.
To further elucidate the mechanism underlying the anti-atherosclerotic effect of Dingxin recipe (DXR).
Fifty 6-week-old male ApoE-/- mice were randomly divided into the following groups: model, simvastatin (5 mg·kg－1·d－1), DXR low-dose (9.30 g·kg－1·d－1), DXR middle-dose (18.59 g·kg－1·d－1) and DXR high-dose (37.18 g·kg－1·d－1) (n = 10). Ten male C57BL/6J mice were used as the control group. All ApoE-/- mice were fed a high-fat diet (HFD) and the control mice received a common diet. After HFD for 12 weeks, the mice were treated with DXR or simvastatin for another 12 weeks. The expression of inflammatory cytokines and visfatin was determined in serum and atherosclerotic lesions by enzyme-linked immunosorbent assay. Visfatin expression was also assessed in aortic atherosclerotic plaques. Cultured vessel endothelial cells (VECs) were pretreated with DXR sera prior to visfatin. The effects of DXR were analyzed to elucidate its protective mechanism against visfatin-induced inflammation in VECs.
DXR regulated blood lipids and reduced tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), intercellular adhesion molecules-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and visfatin expression in ApoE-/- mice, particularly at the higher doses. The areas of atherosclerotic lesions in the DXR groups were significantly smaller than those in the model group. DXR alleviated visfatin-induced VEC injury via downregulation of TNF-α, IL-6, ICAM-1 and VCAM-1 through mitogen-activated protein kinase pathways.
DXR alleviated atherosclerosis injury via downregulation of visfatin expression and inhibition of the visfatin-induced inflammatory response in VECs.
进一步阐明定心方抗动脉粥样硬化作用的机制。
将 50 只 6 周龄雄性 ApoE-/- 小鼠随机分为以下组：模型组、辛伐他汀（5mg·kg－1·d－1）组、定心方低剂量（9.30g·kg－1·d－1）组、定心方中剂量（18.59g·kg－1·d－1）组和定心方高剂量（37.18g·kg－1·d－1）组（n=10）。10 只雄性 C57BL/6J 小鼠作为对照组。所有 ApoE-/- 小鼠均给予高脂饮食（HFD），对照组给予普通饮食。HFD 喂养 12 周后，给予定心方或辛伐他汀治疗 12 周。通过酶联免疫吸附试验测定血清和动脉粥样硬化病变中炎症细胞因子和内脂素的表达。还评估了主动脉粥样硬化斑块中的内脂素表达。用定心方血清预处理培养的血管内皮细胞（VEC），然后分析定心方的作用，以阐明其对 VEC 中内脂素诱导的炎症的保护机制。
定心方调节血脂，降低 ApoE-/- 小鼠肿瘤坏死因子-α（TNF-α）、白细胞介素-6（IL-6）、细胞间黏附分子-1（ICAM-1）、血管细胞黏附分子-1（VCAM-1）和内脂素的表达，尤其是在较高剂量时。定心方组的动脉粥样硬化病变面积明显小于模型组。定心方通过下调 TNF-α、IL-6、ICAM-1 和 VCAM-1 来减轻内脂素诱导的 VEC 损伤，这是通过丝裂原激活蛋白激酶途径实现的。
定心方通过下调内脂素表达和抑制内脂素诱导的 VEC 炎症反应来减轻动脉粥样硬化损伤。
Zotero 插件