Evidence map›Paper›PMID 38017536›Full record

ArticleChinese medicine2023

Salvianolic acid B promotes angiogenesis and inhibits cardiomyocyte apoptosis by regulating autophagy in myocardial ischemia.

Qi Chen, QingYang Xu, Huilin Zhu, Junyi Wang, Ning Sun, Huimin Bian, Yu Li, Chao Lin

Open access · goldAbstract read
In one paragraph

Article in Chinese medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 2 pooled it
6.4field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

24 citing papers in PubMed, 2 syntheses or guidelines pooled it, 30 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Qi Chen *Department of Physiology and Pathophysiology, State Key Laboratory of Medical Neurobiology, School of Basic Medical Sciences, Fudan University, 138 Yi Xue Yuan Road, Shanghai, 200032, People's Republic of China.
QingYang Xu *Department of Physiology and Pathophysiology, State Key Laboratory of Medical Neurobiology, School of Basic Medical Sciences, Fudan University, 138 Yi Xue Yuan Road, Shanghai, 200032, People's Republic of China.
Huilin ZhuSchool of Medicine and Holistic Integrative Medicine, Nanjing University of Chinese Medicine, Nanjing, 210023, China.
Junyi WangSchool of Medicine and Holistic Integrative Medicine, Nanjing University of Chinese Medicine, Nanjing, 210023, China.
Ning SunDepartment of Physiology and Pathophysiology, State Key Laboratory of Medical Neurobiology, School of Basic Medical Sciences, Fudan University, 138 Yi Xue Yuan Road, Shanghai, 200032, People's Republic of China.
Huimin BianSchool of Pharmacy, Nanjing University of Chinese Medicine, Nanjing, 210023, China. hmbian@sina.com.
Yu LiSchool of Medicine and Holistic Integrative Medicine, Nanjing University of Chinese Medicine, Nanjing, 210023, China. liyu@njucm.edu.cn.
Chao LinSchool of Medicine and Holistic Integrative Medicine, Nanjing University of Chinese Medicine, Nanjing, 210023, China. super189lin@163.com.
Nanjing University of Chinese Medicine · CNFudan University · CN

Funding

Jiangsu Provincial Special Program of Medical Science BE2017610National Natural Science Foundation of China 81174029National Natural Science Foundation of China NZY81903927Priority Academic Program Development of Jiangsu Higher Education Institutions JKLPSE201605
6 · The paper itself

Abstract

backgroundMyocardial ischemia (MI) can cause angina, myocardial infarction, and even death. Angiogenesis is beneficial for ensuring oxygen and blood supply to ischemic tissue, promoting tissue repair, and reducing cell damage. In this study, we evaluated the effects of Salvianolic acid B (Sal B) against myocardial ischemia and explored its underlying mechanism on autophagy.

methodsThe anti-apoptosis effect of Sal B was conducted by staining Annexin V-FITC/PI and Hoechst as well as evaluating apoptosis bio-markers at protein level in H9c2 cells at glucose deprivation condition. HUVECs were co-cultured with H9c2, and the tube formation assay was used to monitor Sal B's impact on angiogenesis. The MI model of mice was induced by intraperitoneal injection of isoproterenol (ISO). The effect of Sal B on MI mice was evaluated by HE, Masson, immunohistochemistry, WB and kits. In addition, Atg5 siRNA was applied to verify whether the protective effect of Sal B was regulated to autophagy.

resultsIn H9c2, Sal B reduced the levels of lactate dehydrogenase (LDH), malondialdehyde (MDA) and reactive oxygen species (ROS), improved the levels of superoxide dismutase (SOD) and mitochondrial membrane potential, downregulated the expressions of Bax and cleaved-Caspase3, upregulated the expression of Bcl-2. Therefore, Sal B could significantly inhibit the damage of H9c2 caused by glucose deprivation. In the co-culture system of H9c2 and HUVECs, vascular endothelial growth factor (VEGF) level in the supernatant was dramatically raised by Sal B. Sal B upregulated the expressions of VEGF, platelet derived growth factor (PDGF) and endothelial marker CD31. It implied that Sal B exerted a significant pro-angiogenic effect. Moreover, Sal B increased the expression of LC3, Atg5, and Beclin1, while reducing the level of P62. When the expression of Atg5 was inhibited, the protective effects of Sal B on apoptosis and angiogenesis was reversed.

conclusionsSal B inhibited cardiomyocyte apoptosis and promoted angiogenesis by regulating autophagy, thereby improving MI.

Indexed as

AngiogenesisApoptosisAutophagyMyocardial ischemiaSalvianolic acid B

Identifiers

PMID38017536
PMCPMC10685573
OpenAlexW4389074524

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.