Evidence map›Paper›PMID 38253954›Full record

ArticleIn vitro cellular & developmental biology. Animal2024

Dihydrotanshinone I reduces H9c2 cell damage by regulating AKT and MAPK signaling pathways.

Ya-Chao Wang, Yi-da Shao, Chang-le Shao, Xiao-Qi Guan, Ping-Ping Lu, Ke Ning, Bao-Nian Liu, Hai-Dong Guo

Abstract read
PubMed Publisher
In one paragraph

Article in In vitro cellular & developmental biology. Animal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. Review
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.

Ya-Chao Wang *School of Integrated Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Yi-da Shao *School of Integrated Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Chang-le ShaoSchool of Integrated Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Xiao-Qi GuanSchool of Traditional Chinese Medicine & School of Integrated Chinese and Western Medicine, Nanjing University of Chinese Medicine, Nanjing, China.
Ping-Ping LuSchool of Integrated Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Ke NingSchool of Integrated Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, China. ningke@shutcm.edu.cn.
Bao-Nian LiuSchool of Integrated Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, China. liubaonian@shutcm.edu.cn.
Hai-Dong GuoSchool of Integrated Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, China. hdguo@shutcm.edu.cn.
Shanghai University of Traditional Chinese Medicine · CNNanjing University of Chinese Medicine · CN

Funding

National Natural Science Foundation of China 81970991National Natural Science Foundation of China 82174120Natural Science Foundation of Shanghai Municipality 21ZR1463100Program of Shanghai Academic Research Leader 22XD1423400
6 · The paper itself

Abstract

Cardiovascular disease is the deadliest disease in the world. Previous studies have shown that Dihydrotanshinone I (DHT) can improve cardiac function after myocardial injury. This study aimed to observe the protective effect and mechanism of DHT on H9c2 cells by establishing an oxygen-glucose deprivation/reoxygenation (OGD/R) injury model. By constructing OGD/R injury simulation of H9c2 cells in a myocardial injury model, the proliferation of H9c2 cells treated with DHT concentrations of 0.1 μmol/L were not affected at 24, 48, and 72 h. DHT can significantly reduce the apoptosis of H9c2 cells caused by OGD/R. Compared with the OGD/R group, DHT treatment significantly reduced the level of MDA and increased the level of SOD in cells. DHT treatment of cells can significantly reduce the levels of ROS and Superoxide in mitochondria in H9c2 cells caused by OGD/R and H

Indexed as

FuransHydrogen PeroxidePhenanthrenesProto-Oncogene Proteins c-aktQuinonesAnimalsApoptosisCell LineGlucoseMyocytes, CardiacOxygenSignal Transductiondihydrotanshinone IFuransGlucoseHydrogen PeroxideOxygenPhenanthrenesProto-Oncogene Proteins c-aktQuinonesApoptosisDihydrotanshinone IH9c2 cellsOxidative stressOxygen–glucose deprivation/reoxygenation

Identifiers

PMID38253954
OpenAlexW4391092584

What OpenQuestion holds

Textmetadata
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.