Evidence map›Paper›PMID 27470887›Full record

ArticleZhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology2016

[Role of glucose-6-phosphate dehydrogenase in hepatitis B virus replication and its possible mechanism of action].

Z W Chen, Y H Guan, L N Ma, X Y Liu, Y X Yang, H D Hu, X C Ding, P Hu

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.7field-weighted citation impact, top 17% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. Article
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.

Z W ChenDepartment of Infectious Disease and Emergency Department, General Hospital of Ningxia Medical University, Yinchuan 750004, China.
Y H GuanDepartment of Infectious Disease and Emergency Department, General Hospital of Ningxia Medical University, Yinchuan 750004, China.
L N MaDepartment of Infectious Disease and Emergency Department, General Hospital of Ningxia Medical University, Yinchuan 750004, China.
X Y LiuDepartment of Infectious Disease and Emergency Department, General Hospital of Ningxia Medical University, Yinchuan 750004, China.
Y X YangThe Second Affiliated Hospital of Chongqing Medical University, Chongqing 400010, China.
H D HuThe Second Affiliated Hospital of Chongqing Medical University, Chongqing 400010, China.
X C DingDepartment of Infectious Disease and Emergency Department, General Hospital of Ningxia Medical University, Yinchuan 750004, China.
P HuThe Second Affiliated Hospital of Chongqing Medical University, Chongqing 400010, China.
Chongqing Medical University · CNDalian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo investigate the role of glucose-6-phosphate dehydrogenase (G6PD) in hepatitis B virus (HBV) replication and its possible mechanism of action.

methodsTissue microarray, quantitative real-time PCR, and Western blot were performed to analyze the differences in G6PD expression levels in the HBV-positive and HBV-negative liver tissues, HepG2.2.15 cells, and HepG2 cells. The siRNA transfection technique was used to knock down G6PD gene in HepG2.2.15 cells for 48 hours. Chemiluminescence was used for HBsAg and HBeAg quantification in supernatant, and quantitative real-time PCR was used to measure HBV DNA, type I interferon (IFN), and downstream IFN-stimulated genes. The t-test was used for comparison between groups.

resultsG6PD expression was significantly upregulated in the HBV-positive liver tissues and cells compared with HBV-negative liver tissues and cells, and the stain intensity and immunohistochemical scores were 89.69±54.92 and 31.90±18.62, respectively (P < 0.05). After G6PD expression in HepG2.2.15 cells was interfered by siRNA, the quantitative levels of HBV DNA, HBsAg, and HBeAg in supernatant were reduced significantly, and the mRNA expression levels of IFNα1, IFNβ1, and five downstream IFN-stimulated genes (OAS1, ISG15, OAS3, EIF2α, and PKR) increased significantly (all P < 0.05).

conclusionG6PD plays a vital role in HBV replication, and its mechanism of action in regulating HBV replication may be related to type I IFN signaling pathway.

Indexed as

Virus ReplicationDNA, ViralGene Knockdown TechniquesGlucosephosphate DehydrogenaseHepatitis BHepatitis B e AntigensHepatitis B Surface AntigensHepatitis B virusHep G2 CellsHumansInterferon Type ILiverReal-Time Polymerase Chain ReactionRNA, Small InterferingTransfectionDNA, ViralGlucosephosphate DehydrogenaseHepatitis B e AntigensHepatitis B Surface AntigensInterferon Type IRNA, Small Interfering

Identifiers

PMID27470887
PMCPMC12768976
OpenAlexW2511951628

What OpenQuestion holds

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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.