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丹参酮IIA磺酸钠注射液对中国动脉粥样硬化及动脉粥样硬化性心血管疾病患者促炎细胞因子、黏附分子及趋化因子的影响:一项随机对照试验的荟萃分析

Effects of sodium tanshinone IIA sulfonate injection on pro-inflammatory cytokines, adhesion molecules and chemokines in Chinese patients with atherosclerosis and atherosclerotic cardiovascular disease: a meta-analysis of randomized controlled trials.

作者信息

Xie Fan, Fu Xiaoying, Li Wenbo, Bao Yujin, Chang Feng, Lu Yun, Lu Yuqiong

机构信息

School of International Pharmaceutical Business, China Pharmaceutical University, Nanjing, Jiangsu, China.

出版信息

Front Cardiovasc Med. 2025 Feb 13;12:1511747. doi: 10.3389/fcvm.2025.1511747. eCollection 2025.

DOI:10.3389/fcvm.2025.1511747
PMID:40017522
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11865200/
Abstract

BACKGROUND

Inflammation, as the basic pathogenic mechanism of atherosclerosis, promotes the development of atherosclerosis (AS) and atherosclerotic cardiovascular disease (ASCVD). In numerous experiments based on animal and cellular models, sodium tanshinone IIA sulfonate (STS) injection has been found to reduce the levels of pro-inflammatory cytokines, adhesion molecules, and chemokines in patients with AS and ASCVD, exerting an anti-inflammatory effect to treat the disease.

OBJECTIVES

This study aimed to perform a meta-analysis of randomized controlled trials (RCTs) to quantify the effects of STS on pro-inflammatory cytokines, adhesion molecules, and chemokines in patients with AS and ASCVD.

METHODS

Eight literature databases were searched from inception to January 2024, including PubMed, Web of Science, Cochrane Library, Ebsco, CNKI, VIP, WanFang Data, and ClinicalTrails.gov. Two reviewers independently screened articles and extracted data. The quality of the included studies was assessed using the Cochrane Risk Assessment Tool 2.0. Meta-analysis was performed using RevMan 5.4 software.

RESULTS

Of the 2,698 publications screened, 42 studies were included, and the related trials involved 4,654 Chinese patients. The meta-analysis showed that STS significantly reduced the concentration level of pro-inflammatory cytokines interleukin 6 (IL-6) [standardized mean difference (SMD)=-1.50, 95%CI(-2.06, -0.95),  < 0.00001], tumor necrosis factor-α (TNF-α) [SMD = -2.55, 95%CI(-3.24, -1.86),  < 0.00001], and interleukin-1β (IL-1β) [SMD = -1.21, 95%CI(-2.41, -0.01),  < 0.0001], of adhesion molecules intercellular adhesion molecule-1 (ICAM-1) [SMD = -1.28, 95%CI(-1.55, -1.02),  < 0.00001] and p-selectin [SMD = -1.06, 95%CI(-1.46, -0.67),  < 0.00001], and of chemokines fractalkine [SMD = -1.32, 95%CI(-2.02, -0.61),  = 0.0003] and monocyte chemoattractant protein-1 (MCP-1) [SMD = -0.83, 95%CI(-1.11, -0.55),  < 0.00001] among patients with AS and ASCVD.

CONCLUSION

The use of STS in patients with AS and ASCVD appeared to significantly decrease levels of pro-inflammatory cytokines, adhesion molecules, and chemokines.: [https://www.crd.york.ac.uk/PROSPERO/], PROSPERO [CRD42024496960].

摘要

背景

炎症作为动脉粥样硬化的基本致病机制,促进动脉粥样硬化(AS)和动脉粥样硬化性心血管疾病(ASCVD)的发展。在众多基于动物和细胞模型的实验中,已发现注射丹参酮IIA磺酸钠(STS)可降低AS和ASCVD患者体内促炎细胞因子、黏附分子和趋化因子的水平,发挥抗炎作用以治疗该疾病。

目的

本研究旨在对随机对照试验(RCT)进行荟萃分析,以量化STS对AS和ASCVD患者促炎细胞因子、黏附分子和趋化因子的影响。

方法

检索了从数据库建立至2024年1月的8个文献数据库,包括PubMed、Web of Science、Cochrane Library、Ebsco、中国知网(CNKI)、维普资讯(VIP)、万方数据和ClinicalTrails.gov。两名研究者独立筛选文章并提取数据。使用Cochrane风险评估工具2.0评估纳入研究的质量。采用RevMan 5.4软件进行荟萃分析。

结果

在筛选的2698篇出版物中,纳入了42项研究,相关试验涉及4654名中国患者。荟萃分析表明,STS显著降低了AS和ASCVD患者促炎细胞因子白细胞介素6(IL-6)[标准化均数差(SMD)=-1.50,95%置信区间(CI)(-2.06,-0.95),P<0.00001]、肿瘤坏死因子-α(TNF-α)[SMD = -2.55,95%CI(-3.24,-1.86),P<0.00001]和白细胞介素-1β(IL-1β)[SMD = -1.21,95%CI(-2.41,-0.01),P<0.0001]的浓度水平,黏附分子细胞间黏附分子-1(ICAM-1)[SMD = -1.28,95%CI(-1.55,-1.02),P<0.00001]和P-选择素[SMD = -1.06,95%CI(-1.46,-0.67),P<0.00001]的浓度水平,以及趋化因子 fractalkine[SMD = -1.32,95%CI(-2.02,-0.61),P = 0.0003]和单核细胞趋化蛋白-1(MCP-1)[SMD = -0.83,95%CI(-1.11,-0.55),P<0.00001]的浓度水平。

结论

在AS和ASCVD患者中使用STS似乎可显著降低促炎细胞因子、黏附分子和趋化因子的水平。[https://www.crd.york.ac.uk/PROSPERO/],国际前瞻性系统评价注册库[CRD42024496960]。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5964/11865200/f5af828db5f7/fcvm-12-1511747-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5964/11865200/1490fe3dacd3/fcvm-12-1511747-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5964/11865200/f4f46e659a7a/fcvm-12-1511747-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5964/11865200/324250b0224d/fcvm-12-1511747-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5964/11865200/f5af828db5f7/fcvm-12-1511747-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5964/11865200/1490fe3dacd3/fcvm-12-1511747-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5964/11865200/f4f46e659a7a/fcvm-12-1511747-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5964/11865200/324250b0224d/fcvm-12-1511747-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5964/11865200/f5af828db5f7/fcvm-12-1511747-g004.jpg

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