Evidence map›Paper›PMID 31853618›Full record

ArticleNaunyn-Schmiedeberg's archives of pharmacology2020

Salvianolic acid B protects against myocardial ischaemia-reperfusion injury in rats via inhibiting high mobility group box 1 protein expression through the PI3K/Akt signalling pathway.

Hanqing Liu, Wei Liu, Huiliang Qiu, Dezhi Zou, Huayang Cai, Qiuxiong Chen, Chaoyang Zheng, Danping Xu

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Naunyn-Schmiedeberg's archives of pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 2 pooled it
4.6field-weighted citation impact, top 4% 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

28 citing papers in PubMed, 2 syntheses or guidelines pooled it, 48 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 4 institutions in 1 country.

Hanqing LiuCardiovascular Department, Guangzhou Hospital of integrated Traditional and West Medicine, Guangzhou, 510800, China.
Wei LiuGeriatrics Department, Tongde Hospital of Zhejiang Province, Hangzhou, 310012, Zhejiang, China.
Huiliang QiuSecond Clinical Medical College, Guangzhou University of Chinese Medicine, Guangzhou, 510006, China.
Dezhi ZouEmergency Department, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, 510080, China.
Huayang CaiSecond Clinical Medical College, Guangzhou University of Chinese Medicine, Guangzhou, 510006, China.
Qiuxiong ChenSecond Clinical Medical College, Guangzhou University of Chinese Medicine, Guangzhou, 510006, China.
Chaoyang ZhengSecond Clinical Medical College, Guangzhou University of Chinese Medicine, Guangzhou, 510006, China. zhengchaoyang@medmail.com.
Danping XuSecond Clinical Medical College, Guangzhou University of Chinese Medicine, Guangzhou, 510006, China. 173227223@qq.com.ORCID http://orcid.org/0000-0002-2889-4320
Guangzhou University of Chinese Medicine · CNIntegrated Chinese Medicine (China) · CNSun Yat-sen University · CNTongde Hospital of Zhejiang Province · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Salvianolic acid B (Sal B) has a significant protective effect on myocardial ischaemia-reperfusion (I/R) injury. Therefore, the aims of this study were to determine the effects of Sal B on myocardial ischaemic-reperfusion (I/R) injury in rats and to explore whether its underlying mechanism of cardioprotection occurs through activating the expression of the phosphoinositide 3-kinase/protein, kinase B (PI3K/Akt) and inhibiting the expression of high mobility group protein 1 (HMGB1). Ninety Sprague-Dawley rats were randomized into five groups: group 1 (sham-operated), group 2 (myocardial I/R), group 3 (low dose of Sal B+I/R), group 4 (high dose of Sal B+I/R), and group 5 (high dose of Sal B+I/R+LY294002, which is a specific PI3k inhibitor). All I/R rats received 30 min myocardial ischaemia followed by 24-h reperfusion. Cardiac function, infarct size, myocardial injury marker levels, inflammatory response and cardiomyocyte apoptosis as well as Bcl-2, Bax, P-Akt, HMGB1 and TLR4 expression were measured. In the current study, Sal B significantly ameliorated myocardial I/R injury in a dose-dependent manner, ameliorated cardiac function, reduced myocardial infarction size, decreased myocardial injury marker expression, decreased inflammatory responses, reduced apoptosis, activated PI3K/Akt expression and inhibited HMGB1 expression. However, all effects of Sal B were significantly reversed by LY294002. Overall, the present study indicated that Sal B attenuated myocardial I/R injury by activating PI3K/Akt and inhibiting the release of HMGB1 in rats.

Indexed as

AnimalsApoptosisApoptosis Regulatory ProteinsBenzofuransDepsidesDisease Models, AnimalHMGB1 ProteinInflammation MediatorsMaleMyocardial InfarctionMyocardial Reperfusion InjuryMyocytes, CardiacPhosphatidylinositol 3-KinaseProto-Oncogene Proteins c-aktRats, Sprague-DawleySignal TransductionApoptosis Regulatory ProteinsBenzofuransDepsidesHbp1 protein, ratHMGB1 ProteinInflammation MediatorsPhosphatidylinositol 3-KinaseProto-Oncogene Proteins c-aktsalvianolic acid BMyocardial ischaemia/reperfusion injuryPI3K/Akt/HMGB1Sal B

Identifiers

PMID31853618
PMCPMC7351826
OpenAlexW2995435044

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.