Evidence map›Paper›PMID 30132527›Full record

ArticleMolecular medicine reports2018

Salidroside mitigates hypoxia/reoxygenation injury by alleviating endoplasmic reticulum stress‑induced apoptosis in H9c2 cardiomyocytes.

Meng-Yao Sun, Da-Shi Ma, Song Zhao, Lei Wang, Chun-Ye Ma, Yang Bai

RetractedOpen access · hybridAbstract readRetracted Publication
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

18 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
  2. Article
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  4. Lipotoxicity, ER Stress, and Cardiovascular Disease: Current Understanding and Future Directions.Cardiovascular & hematological agents in medicinal chemistry · 2024
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  15. Article
  16. Antioxidant Effects of Salidroside in the Cardiovascular System.Evidence-based complementary and alternative medicine : eCAM · 2020
    Review
  17. Review
  18. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Meng-Yao SunDepartment of Cardiac Surgery, The First Hospital of Jilin University, Changchun, Jilin 130021, P.R. China.
Da-Shi MaDepartment of Cardiac Surgery, The First Hospital of Jilin University, Changchun, Jilin 130021, P.R. China.
Song ZhaoDepartment of Spine Surgery, The First Hospital of Jilin University, Changchun, Jilin 130021, P.R. China.
Lei WangDepartment of Cardiac Surgery, The First Hospital of Jilin University, Changchun, Jilin 130021, P.R. China.
Chun-Ye MaDepartment of Cardiac Surgery, The First Hospital of Jilin University, Changchun, Jilin 130021, P.R. China.
Yang BaiDepartment of Cardiac Surgery, The First Hospital of Jilin University, Changchun, Jilin 130021, P.R. China.
Jilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endoplasmic reticulum (ER) stress‑induced apoptosis serves a crucial role in the development of myocardial ischemia/reperfusion (I/R) injury. Salidroside is a phenylpropanoid glycoside isolated from Rhodiola rosea L., which is a plant often used in traditional Chinese medicine. It possesses multiple pharmacological actions and protects against myocardial I/R injury in vitro and in vivo. However, it is not yet clear whether ER stress or ER stress‑induced apoptosis contributes to the cardioprotective effects of salidroside against myocardial I/R injury. Hence, hypoxia/reoxygenation (H/R)‑treated H9c2 cardiomyocytes were used in the current study to mimic myocardium I/R injury in vivo. It was hypothesized that salidroside alleviates ER stress and ER stress‑induced apoptosis, thereby reducing H/R injury in H9c2 cells. The results demonstrated that salidroside attenuated H/R‑induced H9c2 cardiomyocyte injury, as cell viability was increased, lactate dehydrogenase release was decreased, morphological changes in apoptotic cells were ameliorated and the apoptosis ratio was reduced compared with the H/R group. ER stress was reversed, indicated by the downregulation of glucose regulated protein 78 and C/EBP homologous protein following pretreatment with salidroside. In addition, salidroside attenuated ER stress‑induced apoptosis, as the expression of cleaved caspase‑12 and pro‑apoptotic protein Bcl‑2 associated X protein and activity of caspase‑3 was decreased, while the expression of anti‑apoptotic protein Bcl‑2 was increased following pretreatment with salidroside. Furthermore, the results indicated that salidroside decreases the activation of the ER stress‑associated signaling pathway, as the expression of phosphorylated protein kinase RNA (PKR)‑like ER kinase (p‑PERK) and phosphorylated inositol‑requiring enzyme‑1α (p‑IRE1α) proteins were decreased following pretreatment with salidroside. These results demonstrate that salidroside protects against H/R injury via regulation of the PERK and IRE1α pathways, resulting in alleviation of ER stress or ER stress‑induced apoptosis in H9c2 cardiomyocytes.

Indexed as

AnimalsApoptosisCardiotonic AgentsCell HypoxiaCell LineEndoplasmic Reticulum StressGlucosidesHypoxiaMyocardial Reperfusion InjuryMyocytes, CardiacPhenolsRatsSignal TransductionCardiotonic AgentsGlucosidesPhenolsrhodioloside

Identifiers

PMID30132527
PMCPMC6131614
OpenAlexW2888626664

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.