Evidence map›Paper›PMID 36321796›Full record

ArticleMolecular medicine reports2022

Ubiquitin‑specific protease 8 ameliorates lipopolysaccharide‑induced spleen injury via suppression of NF‑κB and MAPK signaling pathways.

Wei Bi, Jiawei Zhang, Zhaohao Zeng, Ruiyi Zhou, Jiayi Zhao, Wei Yan, Lu Wang, Xiaoting Li, Lihong Zhu

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.5field-weighted citation impact, top 38% 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

4 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
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  3. Anti-Inflammatory Activity of Peptides fromFoods (Basel, Switzerland) · 2024
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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

9 authors at 3 institutions in 1 country.

Wei Bi *Department of Neurology, The First Affiliated Hospital of Jinan University, Guangzhou, Guangdong 510630, P.R. China.
Jiawei Zhang *Department of Pathophysiology, School of Medicine, Jinan University, Guangzhou, Guangdong 510632, P.R. China.
Zhaohao ZengDepartment of Neurology, The First Affiliated Hospital of Jinan University, Guangzhou, Guangdong 510630, P.R. China.
Ruiyi ZhouDepartment of Neurology, The First Affiliated Hospital of Jinan University, Guangzhou, Guangdong 510630, P.R. China.
Jiayi ZhaoDepartment of Pathophysiology, School of Medicine, Jinan University, Guangzhou, Guangdong 510632, P.R. China.
Wei YanDepartment of Neurology, The First People's Hospital of Kashgar Prefecture, Kashgar, Xinjiang Uygur Autonomous Region 844000, P.R. China.
Lu WangDepartment of Neurology, The First Affiliated Hospital of Jinan University, Guangzhou, Guangdong 510630, P.R. China.
Xiaoting LiDepartment of Neurology, The First Affiliated Hospital of Jinan University, Guangzhou, Guangdong 510630, P.R. China.
Lihong ZhuDepartment of Pathophysiology, School of Medicine, Jinan University, Guangzhou, Guangdong 510632, P.R. China.
First Affiliated Hospital of Jinan University · CNJinan University · CNPeople's Hospital of Xinjiang Uygur Autonomous Region · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In human immunity, the spleen is a major organ, being central to humoral and cellular immunity. In vitro and in vivo, inflammation is regulated by ubiquitin‑specific protease 8 (USP8); however, to the best of our knowledge, the effect of USP8 on spleen injury remains unknown. The present study aimed to investigate the protection offered by USP8 against spleen injury in lipopolysaccharide (LPS)‑induced mice via attenuation of inflammation. A total of 119 C57BL/6J mice were placed into the following groups: Control group, saline group, LPS group, USP8 group, USP8 + LPS group and negative control (NC) + LPS group. A USP8 lentivirus was injected into mice at 1x108 TU/ml intracerebroventricularly for 7 days before LPS was administered via intraperitoneal injection at 750 µg/kg. From each group, serum and spleen samples were collected for analysis. Histological imaging was used to examine the spleen structure. Western blotting was used to detect the expression levels of proteins associated with the mitogen‑activated protein kinase (MAPK) and nuclear factor (NF)‑κB signaling pathways. Pro‑inflammatory cytokines were detected using enzyme‑linked immunosorbent assays. Compared with that in the saline, control and USP8 + LPS groups, the spleen volume in the LPS group was markedly increased, and the width of the splenic cord and sinus exhibited morphological damage in the LPS group. Compared with that in the saline, control and USP8 + LPS groups, the protein expression levels of USP8 in the spleen were decreased in the LPS group. Furthermore, the production of LPS‑induced pro‑inflammatory cytokines (e.g., interleukin‑1β and tumor necrosis factor‑α) was reduced in serum and spleen homogenates by USP8. Related inflammatory pathways, including the NF‑κB and MAPK pathways, were downregulated in the USP8 + LPS group compared with those in the LPS group. In conclusion, the anti‑inflammatory effect of USP8 on LPS‑induced spleen injury may be mediated by the inhibition of MAPK and NF‑κB signaling pathways.

Indexed as

LipopolysaccharidesNF-kappa BAnimalsCytokinesHumansInflammationMiceMice, Inbred C57BLMitogen-Activated Protein KinasesSignal TransductionSpleenUbiquitin-Specific ProteasesCytokinesLipopolysaccharidesMitogen-Activated Protein KinasesNF-kappa BUbiquitin-Specific Proteasesinflammationlipopolysaccharidemitogen-activated protein kinasenuclear factor‑κBspleen injuryubiquitin‑specific protease 8

Identifiers

PMID36321796
PMCPMC9644427
OpenAlexW4307868650

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.