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丹酚酸B在急性缺血性脑卒中治疗中的作用:动物模型的系统评价和荟萃分析

Role of salvianolic acid B in the treatment of acute ischemic stroke: a systematic review and meta-analysis of animal models.

作者信息

Wang Jiashan, Su Pingping, Wan Chenyu, Xu Yingqi, Huang Junyue, Niu Jianli, Jin Zhuqing

机构信息

The Third School of Clinical Medicine, Zhejiang Chinese Medical University, Hangzhou, China.

School of Clinical Medicine, The Affiliated Hospital of Hangzhou Normal University, Hangzhou, Zhejiang, China.

出版信息

Front Pharmacol. 2024 Dec 24;15:1479765. doi: 10.3389/fphar.2024.1479765. eCollection 2024.

DOI:10.3389/fphar.2024.1479765
PMID:39776581
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11705389/
Abstract

BACKGROUND

Salvianolic acid B (Sal B) is potentially the most valuable water-soluble active component in Salvia miltiorrhiza. Its chemical formula contains multiple phenolic hydroxyl groups, so it has a strong antioxidant capacity.

OBJECTIVE

We aim to investigate the efficacy and the potential mechanism of Sal B in the treatment of acute ischemic stroke injury.

MATERIALS AND METHODS

CNKI, VIP, WanFang, SinoMed, PubMed and Web of Science were searched for all the literature related to Sal B in the treatment of acute ischemic stroke before August 2024. The methodological quality was assessed using an inspection scale combining the CAMARADES checklist and the new STAIR criteria. Data were analyzed using RevMan5.4 software.

RESULTS

A total of 14 articles were included. Sal B could effectively reduce infarct size, neurological deficit score, brain edema index, and brain water content in cerebral ischemic animals. Sal B could not only increase the content of superoxide dismutase (SOD) and decrease the content of malondialdehyde (MDA) to achieve anti-oxidative stress, but also reduce the level of interleukin-1β (IL-1β) protein to achieve anti-inflammatory response, and reduce the number of TUNEL cells to reflect its anti-apoptosis effect. In addition, Sal B can improve energy metabolism by increasing the content of energy charge (EC) and phosphocreatine (PCr), and maintaining ion balance via Na/K ATPase activity, resulting in the neuroprotective effects against acute ischemic stroke injury.

CONCLUSION

This study showed that Sal B could significantly protect against acute ischemic stroke injury, mainly through anti-oxidative stress, anti-inflammatory response, anti-apoptosis, improving energy metabolism, and stabilizing ion balance.

摘要

背景

丹酚酸B(Sal B)可能是丹参中最具价值的水溶性活性成分。其化学式含有多个酚羟基,因此具有较强的抗氧化能力。

目的

旨在探讨丹酚酸B治疗急性缺血性脑卒中损伤的疗效及潜在机制。

材料与方法

检索中国知网、维普、万方、中国生物医学文献数据库、PubMed及Web of Science,查找2024年8月前所有与丹酚酸B治疗急性缺血性脑卒中相关的文献。采用结合CAMARADES清单和新的STAIR标准的检查表评估方法学质量。使用RevMan5.4软件进行数据分析。

结果

共纳入14篇文章。丹酚酸B可有效降低脑缺血动物的梗死面积、神经功能缺损评分、脑水肿指数及脑含水量。丹酚酸B不仅可通过增加超氧化物歧化酶(SOD)含量、降低丙二醛(MDA)含量来实现抗氧化应激,还可降低白细胞介素-1β(IL-1β)蛋白水平来实现抗炎反应,减少TUNEL细胞数量以反映其抗凋亡作用。此外,丹酚酸B可通过增加能荷(EC)和磷酸肌酸(PCr)含量改善能量代谢,并通过钠钾ATP酶活性维持离子平衡,从而对急性缺血性脑卒中损伤产生神经保护作用。

结论

本研究表明,丹酚酸B可显著保护急性缺血性脑卒中损伤,主要通过抗氧化应激、抗炎反应、抗凋亡、改善能量代谢及稳定离子平衡实现。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6388/11705389/bf1497730af5/fphar-15-1479765-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6388/11705389/5acea44e63cd/fphar-15-1479765-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6388/11705389/bb4ff7bb9993/fphar-15-1479765-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6388/11705389/f0d9cbeded30/fphar-15-1479765-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6388/11705389/f0eb8a6d4066/fphar-15-1479765-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6388/11705389/5c091a6f1e95/fphar-15-1479765-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6388/11705389/6303ef2f407c/fphar-15-1479765-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6388/11705389/bf1497730af5/fphar-15-1479765-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6388/11705389/5acea44e63cd/fphar-15-1479765-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6388/11705389/f822b25001bc/fphar-15-1479765-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6388/11705389/610e3a6be967/fphar-15-1479765-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6388/11705389/f92719522f40/fphar-15-1479765-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6388/11705389/bb4ff7bb9993/fphar-15-1479765-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6388/11705389/f0d9cbeded30/fphar-15-1479765-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6388/11705389/f0eb8a6d4066/fphar-15-1479765-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6388/11705389/5c091a6f1e95/fphar-15-1479765-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6388/11705389/6303ef2f407c/fphar-15-1479765-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6388/11705389/bf1497730af5/fphar-15-1479765-g010.jpg

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