Evidence map›Paper›PMID 26339453›Full record

ArticleInternational journal of clinical and experimental pathology2015

N-acetylcysteine protects against liver injure induced by carbon tetrachloride via activation of the Nrf2/HO-1 pathway.

Zhaobin Cai, Qi Lou, Fugen Wang, Er Li, Jingjing Sun, Hongying Fang, Jianjun Xi, Liping Ju

Open access · greenAbstract read
In one paragraph

Article in International journal of clinical and experimental pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
11.6field-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

41 citing papers in PubMed, 76 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 2 institutions in 1 country.

Zhaobin CaiXixi Hospital of Hangzhou Affiliated to Zhejiang University of Traditional Chinese Medicine Hangzhou, Zhejiang, People's Republic of China.
Qi LouZhejiang Academy of Medical Sciences Hangzhou, Zhejiang, People's Republic of China.
Fugen WangXixi Hospital of Hangzhou Affiliated to Zhejiang University of Traditional Chinese Medicine Hangzhou, Zhejiang, People's Republic of China.
Er LiXixi Hospital of Hangzhou Affiliated to Zhejiang University of Traditional Chinese Medicine Hangzhou, Zhejiang, People's Republic of China.
Jingjing SunXixi Hospital of Hangzhou Affiliated to Zhejiang University of Traditional Chinese Medicine Hangzhou, Zhejiang, People's Republic of China.
Hongying FangXixi Hospital of Hangzhou Affiliated to Zhejiang University of Traditional Chinese Medicine Hangzhou, Zhejiang, People's Republic of China.
Jianjun XiXixi Hospital of Hangzhou Affiliated to Zhejiang University of Traditional Chinese Medicine Hangzhou, Zhejiang, People's Republic of China.
Liping JuXixi Hospital of Hangzhou Affiliated to Zhejiang University of Traditional Chinese Medicine Hangzhou, Zhejiang, People's Republic of China.
Hangzhou Hospital of Traditional Chinese Medicine · CNZhejiang Academy of Medical Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic liver injury is an important clinical problem which eventually leads to cirrhosis, hepatocellular carcinoma and end-stage liver failure. It is well known that cell damage induced by reactive oxygen species (ROS) is an important mechanism of hepatocyte injure. N-acetylcysteine (NAC), a precursor of glutathione (GSH), is well-known role as the antidote to acetaminophen toxicity in clinic. NAC is now being utilized more widely in the clinical setting for non-acetaminophen (APAP) related causes of liver injure. However, the mechanisms underlying its beneficial effects are poorly defined. Thus, Aim of the present study was to investigate potential hepatic protective role of NAC and to delineate its mechanism of action against carbon tetrachloride (CCl4)-induced liver injury in models of rat. Our results showed that the alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities as well as malondialdehyde (MDA) contents decreased significantly in CCl4-induced rats with NAC treatment. GSH content and superoxide dismutase (SOD) activities remarkably increased in the NAC groups compared with those in CCl4-induced group. Treatment with NAC had been shown to an increase in nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) mRNA levels. In conclusion, these results suggested that NAC upregulated HO-1 through the activation of Nrf2 pathway and protected rat against CCl4-induced liver injure. The results of this study provided pharmacological evidence to support the clinical application of NAC.

Indexed as

AcetylcysteineAnimalsAntioxidantsBiomarkersCarbon TetrachlorideChemical and Drug Induced Liver InjuryCytoprotectionDisease Models, AnimalHeme Oxygenase (Decyclizing)LiverMaleNF-E2-Related Factor 2Oxidative StressRats, Sprague-DawleyRNA, MessengerSignal TransductionAcetylcysteineAntioxidantsBiomarkersCarbon TetrachlorideHeme Oxygenase (Decyclizing)Hmox1 protein, ratNfe2l2 protein, ratNF-E2-Related Factor 2RNA, Messengercarbon tetrachlorideliver injureN-acetylcysteineNrf2/HO-1 pathwayoxidative stress

Identifiers

PMID26339453
PMCPMC4555781
OpenAlexW2405123385

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.