Evidence map›Paper›PMID 33576722›Full record

ArticleInnate immunity2021

Stattic alleviates acute hepatic damage induced by LPS/d-galactosamine in mice.

Sijia Li, Kai Hu, Longjiang Li, Yi Shen, Jiayi Huang, Li Tang, Li Zhang, Ruyue Shao, Han Lu, Yongqiang Yang

Open access · goldAbstract read
In one paragraph

Article in Innate immunity, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.4field-weighted citation impact, top 36% 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

7 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
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  4. Macrophage DGKActa pharmaceutica Sinica. B · 2025
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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

10 authors at 3 institutions in 1 country.

Sijia LiDepartment of Pathophysiology, Chongqing Medical University, China.ORCID 0000-0002-4921-6270
Kai HuDepartment of Pathophysiology, Chongqing Medical University, China.
Longjiang LiDepartment of Pathophysiology, Chongqing Medical University, China.
Yi ShenDepartment of Pathophysiology, Chongqing Medical University, China.
Jiayi HuangDepartment of Pathophysiology, Chongqing Medical University, China.
Li TangDepartment of Pathophysiology, Chongqing Medical University, China.
Li ZhangDepartment of Pathophysiology, Chongqing Medical University, China.
Ruyue ShaoClinical Medical School, Chongqing Medical and Pharmaceutical College, China.ORCID 0000-0001-7714-2427
Han LuDepartment of Anesthesiology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, China.
Yongqiang YangDepartment of Pathophysiology, Chongqing Medical University, China.ORCID 0000-0003-2048-8309
Chongqing Medical University · CNChongqing Medical and Pharmaceutical College · CNShanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Increasing evidence indicates that signal transducer and activator of transcription 3 (STAT3), a vital transcription factor, plays crucial roles in the regulation of inflammation. STAT3 has become a novel therapeutic target for intervention in inflammation-related disorders. However, it remains unclear whether STAT3 plays a part in acute hepatic damage. To investigate the effects of STAT3 here, LPS/d-GalN-induced hepatic damage was induced in mice, the STAT3 inhibitor Stattic was administered, and the degree of liver injury, inflammation, and hepatocyte apoptosis were investigated. The results showed that Stattic mitigated the hepatic morphologic abnormalities and decreased the level of aminotransferase in LPS/D-GalN-insulted mice. The results also indicated that Stattic decreased the levels of TNF-α and IL-6, prevented the activation of the caspase cascade, suppressed cleavage of PARP, and decreased the quantity of TUNEL-positive cells. These results suggest that Stattic provided protective benefits in LPS/d-GalN-induced hepatic damage, and the protective effects might be associated with its anti-inflammatory and anti-apoptotic effects. Therefore, STAT3 might become a novel target for intervening in inflammation-based and apoptosis-based hepatic disorders.

Indexed as

AnimalsAnti-Inflammatory AgentsApoptosisCaspasesCyclic S-OxidesDisease Models, AnimalGalactosamineHumansInterleukin-6LipopolysaccharidesLiverLiver Failure, AcuteMaleMiceMice, Inbred BALB CSTAT3 Transcription FactorAnti-Inflammatory AgentsCaspasesCyclic S-OxidesGalactosamineInterleukin-6LipopolysaccharidesSTAT3 Transcription FactorstatticTumor Necrosis Factor-alphaacute hepatic damageapoptosisinflammationSTAT3Stattic

Identifiers

PMID33576722
PMCPMC7882804
OpenAlexW3127803061

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.