Evidence map›Paper›PMID 33174025›Full record

ArticleMolecular medicine reports2020

Hesperidin ameliorates liver ischemia/reperfusion injury via activation of the Akt pathway.

Shilai Li, Quanlin Qin, Daqing Luo, Wenhui Pan, Yuqing Wei, Yansong Xu, Jijin Zhu, Liming Shang

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
3.4field-weighted citation impact, top 8% 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

12 citing papers in PubMed, 26 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.

Shilai LiDepartment of Emergency, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530021, P.R China.
Quanlin QinDepartment of Emergency, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530021, P.R China.
Daqing LuoDepartment of Emergency, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530021, P.R China.
Wenhui PanDepartment of Emergency, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530021, P.R China.
Yuqing WeiDepartment of Emergency, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530021, P.R China.
Yansong XuDepartment of Emergency, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530021, P.R China.
Jijin ZhuDepartment of Emergency, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530021, P.R China.
Liming ShangDepartment of Hepatobiliary Surgery, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530021, P.R China.
Guangxi Medical University · CNFirst Affiliated Hospital of GuangXi Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hesperidin (HDN) is a bioflavonoid that serves a role as an antioxidant in biological systems. However, although HDN has hydrogen radical‑ and hydrogen peroxide‑removal activities, the role of HDN in liver ischemia/reperfusion (I/R) injury remains unknown. This study aimed to determine the role of HDN in liver I/R injury. Male C57BL/6J wild‑type (WT) mice were subjected to warm partial liver I/R injury. Liver damage was evaluated by measuring serum alanine aminotransferase (ALT) levels, cytokine production, oxidative stress indicators, tissue hematoxylin‑eosin staining and cell death. The Akt signaling pathway was examined to elucidate the underlying mechanisms. HDN had no effect on ALT levels and tissue damage in WT mice without liver I/R injury. However, HDN significantly ameliorated liver I/R injury as measured by serum ALT levels and necrotic tissue areas. HDN decreased malondialdehyde content, but increased the levels of superoxide dismutase, catalase, glutathione peroxidase and glutathione. In addition, HDN significantly attenuated the mRNA expression levels of TNF‑α, IL‑6 and IL‑1β after liver I/R injury. Furthermore, HDN protected the liver against apoptosis in liver I/R injury by increasing the levels of Bcl‑2 and decreasing the levels of cleaved‑caspase 3. Mechanistically, the levels of phosphorylated Akt were elevated by HDN during liver I/R injury. In addition, HDN could induce Akt activation in hepatocytes in vitro. Most importantly, treatment with the Akt inhibitor LY294002 in WT mice blocked the hepatoprotective effects of HDN in liver I/R injury. In summary, the results of the present study suggested that HDN may protect against liver I/R injury through activating the Akt pathway by ameliorating liver oxidative stress, suppressing inflammation and preventing hepatocyte apoptosis. HDN may be a useful factor for liver injury protection and a potential therapeutic treatment for liver I/R injury in the future.

Indexed as

Alanine TransaminaseAnimalsAntioxidantsApoptosisChinaHepatocytesHesperidinIschemiaLiverLiver DiseasesMaleMalondialdehydeMiceMice, Inbred C57BLOxidative StressPhosphatidylinositol 3-KinasesAlanine TransaminaseAntioxidantsHesperidinMalondialdehydePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTumor Necrosis Factor-alpha

Identifiers

PMID33174025
PMCPMC7646746
OpenAlexW3091915012

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.