清心解瘀颗粒抗动脉粥样硬化的药效学及调控机制

doi:10.12122/j.issn.1673-4254.2024.08.10

南方医科大学学报 ›› 2024, Vol. 44 ›› Issue (8): 1518-1528.doi: 10.12122/j.issn.1673-4254.2024.08.10

• • 上一篇

清心解瘀颗粒抗动脉粥样硬化的药效学及调控机制

张珊苑¹(), 蔡巧燕¹^,²^,⁴(), 祁江晗¹, 殷恺馨³, 何晨晨¹, 高铸烨⁵, 张铃¹^,²^,⁴(), 褚剑锋¹^,²^,⁴()

^1.福建中医药大学，中西医结合学院//中西医结合研究院，福建福州 350122
^2.福建中医药大学，陈可冀学术思想传承工作室，福建福州 350122
^3.福建中医药大学，康复医学院，福建福州 350122
^4.福建省中西医结合老年性疾病重点实验室，福建福州 350122
^5.中国中医科学院西苑医院，北京 100091

收稿日期:2024-05-17 出版日期:2024-08-20 发布日期:2024-09-06
通讯作者: 张铃,褚剑锋 E-mail:shanyuanzhang66@gmail.com;cqy2005899@163.com;remona1986@126.com;jianfengchu@126.com
作者简介:张珊苑，在读硕士研究生，E-mail: shanyuanzhang66@gmail.com
蔡巧燕，博士，高级实验师，E-mail: cqy2005899@163.com
第一联系人：张珊苑、蔡巧燕共同为第一作者
基金资助:
福建省科学技术厅中央引导地方科技发展专项(2021L3014)

Pharmacodynamics of Qingxin Jieyu Granules for treatment of atherosclerosis and its regulatory mechanism for lipid metabolism

Shanyuan ZHANG¹(), Qiaoyan CAI¹^,²^,⁴(), Jianghan QI¹, Kaixin YIN³, Chenchen HE¹, Zhuye GAO⁵, Ling ZHANG¹^,²^,⁴(), Jianfeng CHU¹^,²^,⁴()

^1.College of Integrative Medicine//Academy of Integrative Medicine,
^2.Chen Keji Academic Thought Inheritance Studio,
^3.College of Rehabilitation Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou 350122, China
^4.Fujian Provincial Key Laboratory of Integrative Medicine on Geriatrics, Fuzhou 350122, China
^5.Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing 100091, China

Received:2024-05-17 Online:2024-08-20 Published:2024-09-06
Contact: Ling ZHANG, Jianfeng CHU E-mail:shanyuanzhang66@gmail.com;cqy2005899@163.com;remona1986@126.com;jianfengchu@126.com

摘要/Abstract

摘要：

目的基于网络药理学探讨清心解瘀颗粒（QXJYG）抗动脉粥样硬化（AS）的药效学及其调控机制。方法通过网络药理学挖掘QXJYG抗AS的关键靶点和信号通路。采用高脂喂养合并腹腔注射维生素D3的方式构建AS大鼠模型，将造模成功后的30只大鼠随机分为模型组、阿托伐他汀组（13.15 mg·kg^-1·d^-1）、低剂量组（0.99 g·kg^-1·d^-1）、中剂量组（1.98 g·kg^-1·d^-1）、高剂量组（3.96 g·kg^-1·d^-1），每组6只；另外将6只SD大鼠给予正常饮食作为对照组。实验动物干预8周后，通过小动物超声检测大鼠腹主动脉血管内径、血管壁厚度、脉冲波传播速度、搏动指数，通过HE染色检测大鼠腹主动脉病理形态，通过全自动生化仪检测每组大鼠的血脂水平，通过ELISA检测试剂盒测定血清中AngⅡ、ET-1、TXA2、PGI2、ox-LDL含量。采用免疫组化法检测大鼠腹主动脉中LOX-1、PPARγ、RXRα、p-P65、VCAM-1、ICAM-1蛋白的表达。结果与正常组相比，模型组的腹主动脉血管壁厚度、脉冲波传播速度、搏动指数升高（P<0.05），血管内径减小（P<0.05），且平滑肌细胞增生、排列紊乱，TC、LDL-C、AngⅡ、ET-1、TXA2含量显著升高（P<0.05），HDL-C、PGI2含量显著下降（P<0.05）。与模型组相比，QXJYG和阿托伐他汀干预后，显著降低腹主动脉血管壁厚度、脉冲波传播速度、搏动指数（P<0.05），增大血管内径（P<0.05），减轻平滑肌细胞排列紊乱情况，显著降低TC、LDL-C，AngⅡ、ET-1、TXA2（P<0.05），显著升高HDL-C、PGI2含量（P<0.05），通过网络药理学预测发现QXJYG可能通过调控脂质，PPAR和NF-κB等信号通路发挥抗AS的作用。与正常组相比，模型组的ox-LDL含量、LOX-1、p-P65、VCAM-1、ICAM-1蛋白表达水平显著升高（P<0.05），PPARγ、RXRα蛋白表达水平明显降低（P<0.05）；与模型组相比，QXJYG干预后，ox-LDL含量、LOX-1、p-P65、VCAM-1、ICAM-1蛋白表达水平显著降低（P<0.05），PPARγ、RXRα表达显著升高（P<0.05）。结论 QXJYG显著改善AS大鼠脂代谢紊乱，扩大腹主动脉血管内径，减小腹主动脉血管壁厚度，抑制腹主动脉血管病理损伤，调节血管收缩和舒张功能。QXJYG发挥抗AS的作用机制可能是抑制血脂中ox-LDL水平，降低LOX-1的表达，激活PPARγ、RXRα蛋白，抑制P65的磷酸化，从而降低VCAM-1、ICAM-1蛋白表达。

关键词: 清心解瘀颗粒, 动脉粥样硬化, 网络药理学, PPARγ/RXRα信号通路, NF-κB信号通路

Abstract:

Objective To elucidate the therapeutic mechanism of Qingxin Jieyu Granule (QXJYG) against atherosclerosis (AS) based on network pharmacology. Methods The major targets and pathways of QXJYG against AS were analyzed using network pharmacology. Rat models of AS established by high-fat feeding combined with intraperitoneal vitamin D3 injection were treated daily with normal saline, atorvastatin (13.15 mg/kg), or QXJYG at 0.99, 1.98, and 3.96 g/kg for 8 weeks (n=6). Ultrasound and HE staining were used to assess the function and pathologies of the abdominal aorta. Blood lipids and serum levels of Ang II, ET-1, TXA2, PGI2, and ox-LDL of the rats were detected using an automatic biochemical analyzer or ELISA. The expressions of LOX-1, PPARγ, RXRα, p-P65, VCAM-1 and ICAM-1 in the abdominal aorta were detected with immunohistochemistry. Results The rat models of AS showed obvious abdominal aorta wall thickening, increased pulse wave velocity and pulse index, decreased inner diameter of the abdominal aorta, elevated levels of TC, LDL-C, Ang II, ET-1 and TXA2, and lowered levels of HDL-C and PGI2. QXJYG and atorvastatin treatment of the rat models significantly alleviated histopathological changes of the abdominal aorta, decreased serum levels of TC, LDL-C, Ang II, ET-1 and TXA2, and increased the levels of HDL-C and PGI2. Network pharmacology study suggested the therapeutic effect of QXJYG against AS was mediated by regulating lipid metabolism, PPAR and NF‑κB pathways. Consistently, treatments with QXJYG were found to significantly decrease ox-LDL level and LOX-1, P-P65, VCAM-1 and ICAM-1 protein expressions while increasing PPARγ and RXRα expressions in the aorta of AS rats. Conclusion QXJYG alleviates lipid metabolism disorder and improves histopathological changes of the abdominal aorta of AS rats possibly by lowering ox-LDL level, reducing LOX-1 expression, activating PPARγ and RXRα, and inhibiting P65 phosphorylation to reduce VCAM-1 and ICAM-1 expression in the aorta.

Key words: Qingxin Jieyu Granule, atherosclerosis, network pharmacology, PPARγ/RXRα signaling pathway, NF-κB signaling pathway

张珊苑, 蔡巧燕, 祁江晗, 殷恺馨, 何晨晨, 高铸烨, 张铃, 褚剑锋. 清心解瘀颗粒抗动脉粥样硬化的药效学及调控机制[J]. 南方医科大学学报, 2024, 44(8): 1518-1528.

Shanyuan ZHANG, Qiaoyan CAI, Jianghan QI, Kaixin YIN, Chenchen HE, Zhuye GAO, Ling ZHANG, Jianfeng CHU. Pharmacodynamics of Qingxin Jieyu Granules for treatment of atherosclerosis and its regulatory mechanism for lipid metabolism[J]. Journal of Southern Medical University, 2024, 44(8): 1518-1528.

图/表 10

图1 清心解瘀颗粒对动脉粥样硬化大鼠血管壁厚度、脉冲波传播速度、搏动指数和血管内径的影响

Fig.1 Effects of QXJYG on vessel wall thickness, pulse wave propagation velocity, pulsatility index and vessel diameter in atherosclerotic rats. A, B: Ultrasound images and quantitative comparison of wall thickness of the abdominal aorta. C, D: Sonograms and quantitative comparison of pulse-wave propagation velocity of the abdominal aorta. E, F: Echocardiograms and quantitative analysis of the pulsatility index of the abdominal aorta. G, H: Ultrasound images and quantitative analysis of abdominal aorta vessel diameter. LPT: Positive control (atorvastatin) group; LD: Low-dose QXJYG group; MD: Medium-dose QXJYG group; HD: High-dose QXJYG group. *P<0.05 vs Control group; #P<0.05 vs Model group; △P<0.05 vs LD group; &P<0.05 vs MD group.

图2 清心解瘀颗粒对动脉粥样硬化大鼠腹主动脉血管病理情况的影响

Fig.2 Effects of QXJYG on vascular pathology of the abdominal aorta in rats with atherosclerosis (HE staining, Scale bar=50 µm).①Intimal thickening of the blood vessels; ②Proliferation of smooth muscle cells with disordered arrangement.

图3 清心解瘀颗粒对动脉粥样硬化大鼠血清中TC、LDL-C、TG、HDL-C含量的影响

Fig.3 Effects of QXJYG on serum levels of TC, LDL-C, TG and HDL-C in rats with atherosclerosis. A: Serum levels of TC and LDL-C. B: Serum levels of TG and HDL-C. *P<0.05 vs Control group; #P<0.05 vs Model group; △P<0.05 vs LD group.

图4 清心解瘀颗粒对动脉粥样硬化大鼠血清中AngⅡ、ET-1、TXA2、PGI2含量的影响

Fig.4 Effects of QXJYG on serum levels of Ang II (A), ET-1 (B), TXA2 (C) and PGI2 (D) in rats with atherosclerosis. *P<0.05 vs Control group; #P<0.05 vs Model group; △P<0.05 vs LD group; &P<0.05 vs MD group.

图5 清心解瘀颗粒与动脉粥样硬化作用靶点分析图

Fig.5 Analysis of targets of QXJYG and AS. A: Quantity diagram of each drug compound of QXJYG. B: Number of drug targets of QXJYG. C: Venn diagram of QXJYG and AS targets. D: PPI plot of potential protein interaction of QXJYG against AS.

表1 清心解瘀颗粒抗动脉粥样硬化度值高于平均值的交叉靶点

Tab.1 Cross targets of QXJYG with anti-AS values higher than the average value

Key target	Degree	Betweenness centrality	Closeness centrality
IL-6	21	0.14771628	0.83870968
IL-1B	19	0.0880959	0.78787879
PPARG	19	0.20820912	0.78787879
VCAM1	16	0.03766667	0.7027027
IL-10	14	0.02131169	0.66666667
SERPINE1	14	0.01293806	0.65
ESR1	14	0.04946542	0.65
SPP1	14	0.01452414	0.65
CRP	13	0.00772194	0.63414634
SIRT1	13	0.04028405	0.65
NOS3	13	0.01529604	0.63414634
MMP3	11	0.00423576	0.57777778
SELE	10	0.00117216	0.59090909

图6 清心解瘀颗粒抗动脉粥样硬化的KEGG通路富集分析与GO功能分析

Fig.6 KEGG pathway enrichment analysis and GO functional analysis of QXJYG against AS.A: KEGG pathway enrichment analysis of QXJYG against AS. B: Biological processes analysis of QXJYG against AS. C: Cell components analysis of QXJYG against AS. D: Molecular function analysis of QXJYG against AS.

图7 清心解瘀颗粒对动脉粥样硬化大鼠血清中ox-LDL的影响

Fig.7 Effect of QXJYG on serum ox-LDL in atherosclerotic rats. *P<0.05 vs Control group; #P<0.05 vs Model group; △P<0.05 vs LD group.

图8 清心解瘀颗粒对动脉粥样硬化大鼠腹主动脉中LOX-1、PPARγ、RXRα、p-P65蛋白表达的影响

Fig.8 Effect of QXJYG on the expression of LOX-1, PPARγ, RXRα and p-P65 in the abdominal aorta of atherosclerotic rats (DAB staining, original magnification: ×400). A, B: LOX-1 expression and positivity rate in the abdominal aorta. C, D: PPARγ expression and positivity rate in the abdominal aorta. E, F: Expression of RXRα and positivity rate positive rate. G, H: Expression of p-P65 and positivity rate. *P<0.05 vs Control group; #P<0.05 vs Model group; △P<0.05 vs LD group; &P<0.05 vs MD group.

图9 清心解瘀颗粒对动脉粥样硬化大鼠腹主动脉中VCAM-1、ICAM-1蛋白表达的影响

Fig.9 Effect of QXJYG on the expression of VCAM-1 and ICAM-1 in abdominal aorta of atherosclerotic rats (DAB staining, ×400). A, B: VCAM-1 expression and positivity rate in the abdominal aorta. C, D: ICAM-1 expression and positivity rate in the abdominal aorta. *P<0.05 vs Control group; #P<0.05 vs Model group; △P<0.05 vs LD group.

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清心解瘀颗粒抗动脉粥样硬化的药效学及调控机制

Pharmacodynamics of Qingxin Jieyu Granules for treatment of atherosclerosis and its regulatory mechanism for lipid metabolism

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