Evidence map›Paper›PMID 28905500›Full record

ArticleJournal of cellular and molecular medicine2017

Salidroside suppressing LPS-induced myocardial injury by inhibiting ROS-mediated PI3K/Akt/mTOR pathway in vitro and in vivo.

Lvyi Chen, Peng Liu, Xin Feng, Chunhua Ma

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 135 papers.

0numbers the graph read from it
0cells of the map it votes in
135citing papers in PubMed
5.1field-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

135 citing papers in PubMed, 250 citations in OpenAlex.

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75 more citing papers are in PubMed but not listed here.

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

4 authors at 3 institutions in 1 country.

Lvyi ChenSchool of Pharmacy, South-Central University for Nationalities, Wuhan, China.
Peng LiuSchool of Pharmacy, South-Central University for Nationalities, Wuhan, China.
Xin FengInstitute of Tibetan Medicine, China Tibetology Research Center, Beijing, China.
Chunhua MaDepartment of Physiology and Pharmacology, China Pharmaceutical University, Nanjing, China.
South Central University for Nationalities · CNChina Pharmaceutical University · CNChina Tibetology Research Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The purpose of the present study was to investigate the effect of salidroside (Sal) on myocardial injury in lipopolysaccharide (LPS)-induced endotoxemic in vitro and in vivo. SD rats were randomly divided into five groups: control group, LPS group (15 mg/kg), LPS plus dexamethasone (2 mg/kg), LPS plus Sal groups with different Sal doses (20, 40 mg/kg). Hemodynamic measurement and haematoxylin and eosin staining were performed. Serum levels of creatine kinase (CK), lactate dehydrogenase, the activities of the antioxidant enzymes catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GSH-px), glutathione, tumour necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β) were measured after the rats were killed. iNOS, COX-2, NF-κB and PI3K/Akt/mTOR pathway proteins were detected by Western blot. In vitro, we evaluated the protective effect of Sal on rat embryonic heart-derived myogenic cell line H9c2 induced by LPS. Reactive oxygen species (ROS) in H9c2 cells was measured by flow cytometry, and the activities of the antioxidant enzymes CAT, SOD, GSH-px, glutathione-S-transferase, TNF-α, IL-6 and IL-1β in cellular supernatant were measured. PI3K/Akt/mTOR signalling was examined by Western blot. As a result, Sal significantly attenuated the above indices. In addition, Sal exerts pronounced cardioprotective effect in rats subjected to LPS possibly through inhibiting the iNOS, COX-2, NF-κB and PI3K/Akt/mTOR pathway in vivo. Furthermore, the pharmacological effect of Sal associated with the ROS-mediated PI3K/Akt/mTOR pathway was proved by the use of ROS scavenger, N-acetyl-l-cysteine, in LPS-stimulated H9C2 cells. Our results indicated that Sal could be a potential therapeutic agent for the treatment of cardiovascular disease.

Indexed as

AnimalsCardiotonic AgentsCatalaseCell LineDexamethasoneEndotoxemiaGene Expression RegulationGlucosidesGlutathioneGlutathione PeroxidaseHemodynamicsInterleukin-1betaInterleukin-6LipopolysaccharidesMyocardial Reperfusion InjuryMyocardiumCardiotonic AgentsCatalaseDexamethasoneGlucosidesGlutathioneGlutathione PeroxidaseIL1B protein, ratInterleukin-1betaInterleukin-6LipopolysaccharidesmTOR protein, ratNitric Oxide Synthase Type IINos2 protein, ratPhenolsPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-aktReactive Oxygen SpeciesrhodiolosideSuperoxide DismutaseTOR Serine-Threonine KinasesTumor Necrosis Factor-alphaH9C2LPSmyocardial injuryPI3K/Akt/mTORROSsalidroside

Identifiers

PMID28905500
PMCPMC5706507
OpenAlexW2754559965

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.