Evidence map›Paper›PMID 36063304›Full record

ArticleInflammopharmacology2022

Escin suppresses immune cell infiltration and selectively modulates Nrf2/HO-1, TNF-α/JNK, and IL-22/STAT3 signaling pathways in concanavalin A-induced autoimmune hepatitis in mice.

Mahmoud Elshal, Sara H Hazem

Open access · hybridAbstract read
In one paragraph

Article in Inflammopharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

22 citing papers in PubMed, 26 citations in OpenAlex.

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  17. IL-22, a vital cytokine in autoimmune diseases.Clinical and experimental immunology · 2024
    Review
  18. Review
  19. Optimization of Enzyme-Assisted Extraction from Ginger (Preventive nutrition and food science · 2024
    Article
  20. Review
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

2 authors at 1 institution in 1 country.

Mahmoud ElshalDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, Mansoura University, ElGomhoria Street, Mansoura, 35516, Egypt. mahmoudelshal@mans.edu.eg.ORCID http://orcid.org/0000-0002-9528-7483
Sara H HazemDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, Mansoura University, ElGomhoria Street, Mansoura, 35516, Egypt.
Mansoura University · EG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The current study aims to investigate the possible protective effect of escin, the active constituent of a natural mixture of triterpene saponin glycoside, against immune-mediated hepatitis driven by concanavalin A (Con A) and to elucidate its possible underlying mechanisms. Adult male mice were administered Con A (15 mg/kg, intravenously) for 8 h. In the treated groups, mice were pretreated with escin daily (10 mg/kg in CMC, orally) for 4 days before Con A intoxication. In addition, escin was administered in a group to examine its effect on normal mice. Our results showed that escin inhibited Con A-induced elevation in liver enzymes (ALT, AST, and LDH) and curbed the Con A-induced hepatocyte necrosis and apoptosis together with abrogating the death pathway, JNK. Coincidentally, escin has shown a reduction in neutrophil, CD4+ T cell, and monocyte infiltration into the liver. In addition, escin modulated the cellular oxidant status by compensating for the Con A-depleted expression of the transcription factor Nrf2 and the stress protein hemeoxygenase-1. These effects were in good agreement with the restraining effect of escin on Con A-instigated overexpression of NF-κB and the pro-inflammatory cytokines TNF-α and IL-17A. Interestingly, Con A provoked the cellular protective pathway IL-22/STAT3, which was revoked by the escin pretreatment. In conclusion, escin shows extended antioxidant, anti-inflammatory, antinecrotic, and anti-apoptotic effects against Con A-induced immune-mediated hepatitis. These effects may collectively be via suppressing immune cell infiltration into the liver and selective modulation of Nrf2/HO-1, TNF-α/NF-κB, TNF-α/JNK, and IL-22/STAT3 signaling pathways.

Indexed as

EscinHepatitis, AutoimmuneAnimalsConcanavalin ACytokinesInterleukin-22LiverMaleMiceNF-E2-Related Factor 2NF-kappa BSignal TransductionTumor Necrosis Factor-alphaConcanavalin ACytokinesEscinInterleukin-22NF-E2-Related Factor 2NF-kappa BTumor Necrosis Factor-alphaCD4+Concanavalin AEscinIL-22JNKNrf2

Identifiers

PMID36063304
PMCPMC9700661
OpenAlexW4294597705

What OpenQuestion holds

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LicenceCC BY
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.