Evidence map›Paper›PMID 29321061›Full record

ArticleBMC pharmacology & toxicology2018

Enoxaparin attenuates doxorubicin induced cardiotoxicity in rats via interfering with oxidative stress, inflammation and apoptosis.

Reem Ali Shaker, Samer Hassan Abboud, Hayder Chasib Assad, Najah Hadi

Open access · goldAbstract read
In one paragraph

Article in BMC pharmacology & toxicology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
11.1field-weighted citation impact, top 1% 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

44 citing papers in PubMed, 125 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

4 authors at 2 institutions in 1 country.

Reem Ali ShakerNajaf Health Directorate, Ministry of Health, Najaf Governorate, Iraq.
Samer Hassan AbboudFaculty of Medicine, University of Kufa, Najaf Governorate, Iraq.
Hayder Chasib AssadDepartment of Clinical Pharmacy and Therapeutics, Faculty of Pharmacy, University of Kufa, Najaf Governorate, Iraq. hayderc.allami@uokufa.edu.iq.
Najah HadiFaculty of Medicine, University of Kufa, Najaf Governorate, Iraq.
University of Kufa · IQMinistry of Health · IQ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDoxorubicin (DOX) is commonly used in the treatment of many types of cancers but its cardiotoxicity is limiting its clinical use. Beyond its anticoagulant action, enoxaparin (ENX), a low molecular weight heparin, has been shown to exert multiple pharmacological actions including antioxidant, anti-inflammatory and antiapoptotic effects. Therefore, the current study aimed to assess if ENX could ameliorate cardiotoxicity induced by DOX.

methodsTwenty-one adult male Wistar albino rats were randomly allocated into three groups (n = 7 each) of control, receiving 0.9% saline (i.p.), DOX, receiving 2.5 mg/kg of DOX (i.p.) thrice weekly; and DOX + ENX, receiving ENX (250 IU/kg/day i.p.) and a DOX dose equivalent to that of the DOX only group.

resultsDOX-induced cardiotoxicity was indicated by marked increases in cardiac troponin I (cTnI) and severe histological lesions, which significantly correlated with cardiotoxicity, oxidative stress, inflammation and apoptosis markers, compared to controls. DOX group also showed elevations in malondialdehyde (MDA), a marker of oxidative stress, and reductions in total antioxidant capacity (TAC). Cardiac inflammatory markers including tumor necrosis factor alpha (TNF-α) and interleukin-1 beta (IL-1β) and caspase-3, an apoptotic marker, were also elevated in the DOX group. DOX, however, did not significantly alter brain natriuretic peptide (BNP) levels. ENX significantly attenuated, but not completely reversed, DOX-induced cardiotoxicity through lowering cTnI and improving cardiomyopathy histopathological scores as compared to the DOX group. ENX also decreased MDA, increased TAC of rats' heart to levels relatively comparable to control. Significant reductions in TNF-α, IL-1β and caspase-3 were also observed following ENX treatment relative to the DOX only group.

conclusionsCollectively, these results describe a cardioprotective effect for ENX against DOX-induced cardiotoxicity which is likely facilitated via suppression of oxidative stress, inflammation and apoptosis.

Indexed as

AnimalsAntibiotics, AntineoplasticApoptosisCardiotonic AgentsCardiotoxicityDoxorubicinEnoxaparinInflammationMaleMyocardiumOxidative StressRats, WistarAntibiotics, AntineoplasticCardiotonic AgentsDoxorubicinEnoxaparinAntioxidantCardiotoxicityDoxorubicinInflammatory markers and caspase-3Low molecular weight heparin

Identifiers

PMID29321061
PMCPMC5763526
OpenAlexW2783983996

What OpenQuestion holds

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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.