Evidence map›Paper›PMID 25083879›Full record

ArticlePloS one2014

Carvacrol alleviates ischemia reperfusion injury by regulating the PI3K-Akt pathway in rats.

Lida Suo, Kai Kang, Xun Wang, Yonggang Cao, Haifeng Zhao, Xueying Sun, Liquan Tong, Feng Zhang

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
3.8field-weighted citation impact, top 7% 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

16 citing papers in PubMed, 47 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.

Lida SuoDepartment of General Surgery, the Fifth Affiliated Hospital of Harbin Medical University, Daqing, Heilongjiang Province, China.
Kai KangDepartment of General Surgery, the Fifth Affiliated Hospital of Harbin Medical University, Daqing, Heilongjiang Province, China.
Xun WangDepartment of General Surgery, Daqing Oilfield General Hospital, Daqing, Heilongjiang Province, China.
Yonggang CaoDepartment of Pharmacology, Daqing Campus of Harbin Medical University, Daqing, Heilongjiang Province, China.
Haifeng ZhaoDepartment of General Surgery, the Fifth Affiliated Hospital of Harbin Medical University, Daqing, Heilongjiang Province, China.
Xueying SunThe Hepatosplenic Surgery Center, Department of General Surgery, the First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang Province, China.
Liquan TongDepartment of General Surgery, the Fifth Affiliated Hospital of Harbin Medical University, Daqing, Heilongjiang Province, China.
Feng ZhangDepartment of General Surgery, the Fifth Affiliated Hospital of Harbin Medical University, Daqing, Heilongjiang Province, China.
Daqing City People's Hospital · CNHarbin Medical University · CNDaqing Oilfield General Hospital · CNFirst Affiliated Hospital of Harbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLiver ischemia reperfusion (I/R) injury is a common pathophysiological process in many clinical settings. Carvacrol, a food additive commonly used in essential oils, has displayed antimicrobials, antitumor and antidepressant-like activities. In the present study, we investigated the protective effects of carvacrol on I/R injury in the Wistar rat livers and an in vitro hypoxia/restoration (H/R) model.

methodsThe hepatoportal vein, hepatic arterial and hepatic duct of Wistar rats were isolated and clamped for 30 min, followed by a 2 h reperfusion. Buffalo rat liver (BRL) cells were incubated under hypoxia for 4 h, followed normoxic conditions for 10 h to establish the H/R model in vitro. Liver injury was evaluated by measuring serum levels of alanine aminotransferase (ALT) and aspatate aminotransferase (AST), and hepatic levels of superoxide dismutase (SOD), catalase (CAT), glutathione (GSH) and malondiadehyde (MDA), and hepatic histology and TUNEL staining. MTT assay, flow cytometric analysis and Hoechst 33258 staining were used to evaluate the proliferation and apoptosis of BRL cells in vitro. Protein expression was examined by Western Blot analysis.

resultsCarvacrol protected against I/R-induced liver damage, evidenced by significantly reducing the serum levels of ALT and AST, histological alterations and apoptosis of liver cells in I/R rats. Carvacrol exhibited anti-oxidative activity in the I/R rats, reflected by significantly reducing the activity of SOD and the content of MDA, and restoring the activity of CAT and the content of GSH, in I/R rats. In the in vitro assays, carvacrol restored the viability and inhibited the apoptosis of BRL cells, which were subjected to a mimic I/R injury induced by hypoxia. In the investigation on molecular mechanisms, carvacrol downregulated the expression of Bax and upregulated the expression of Bcl-2, thus inhibited the activation of caspase-3. Carvacrol was also shown to enhance the phosphorylation of Akt.

conclusionThe results suggest that carvacrol could alleviate I/R-induced liver injury by its anti-oxidative and anti-apoptotic activities, and warrant a further investigation for using carvacrol to protect I/R injury in clinic.

Indexed as

Signal TransductionAlanine TransaminaseAnimalsAntioxidantsApoptosisAspartate Aminotransferasesbcl-2-Associated X ProteinBlotting, WesternCaspase 3Cell LineCell SurvivalCymenesHepatocytesMaleMonoterpenesPhosphatidylinositol 3-KinasesAlanine TransaminaseAntioxidantsAspartate Aminotransferasesbcl-2-Associated X ProteincarvacrolCaspase 3CymenesMonoterpenesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-akt

Identifiers

PMID25083879
PMCPMC4118998
OpenAlexW1976693938

What OpenQuestion holds

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LicenceCC BY
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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.