Evidence map›Paper›PMID 31611735›Full record

ArticleMediators of inflammation2019

Protective Effects of Oridonin on Acute Liver Injury via Impeding Posttranslational Modifications of Interleukin-1 Receptor-Associated Kinase 4 (IRAK4) in the Toll-Like Receptor 4 (TLR4) Signaling Pathway.

Min Shi, Yilin Deng, Heguo Yu, Ling Xu, Cuicui Shi, Jiong Chen, Guangming Li, Yiqi Du, Yu-Gang Wang

Open access · goldAbstract read
In one paragraph

Article in Mediators of inflammation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.5field-weighted citation impact, top 35% 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

6 citing papers in PubMed, 19 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

9 authors at 4 institutions in 1 country.

Min ShiDepartment of Gastroenterology, Changhai Hospital, Second Military Medical University/Naval Medical University, Shanghai 200433, China.ORCID https://orcid.org/0000-0002-2130-181X
Yilin DengDepartment of Gastrointestinal Cancer Biology, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin 300060, China.
Heguo YuNPFPC Key Laboratory of Contraceptives and Devices, Shanghai Institute of Planned Parenthood Research (SIPPR), Institutes of Reproduction and Development, Fudan University, Shanghai 200000, China.ORCID https://orcid.org/0000-0001-8425-8137
Ling XuDepartment of Gastroenterology, Shanghai Tongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200336, China.ORCID https://orcid.org/0000-0002-3438-8432
Cuicui ShiDepartment of Gastroenterology, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200092, China.
Jiong ChenDepartment of Gastroenterology, Shanghai Tongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200336, China.
Guangming LiDepartment of Gastroenterology, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200092, China.ORCID https://orcid.org/0000-0003-2977-4598
Yiqi DuDepartment of Gastroenterology, Changhai Hospital, Second Military Medical University/Naval Medical University, Shanghai 200433, China.ORCID https://orcid.org/0000-0002-4261-6888
Yu-Gang WangDepartment of Gastroenterology, Shanghai Tongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200336, China.ORCID https://orcid.org/0000-0001-5675-2509
Shanghai Jiao Tong University · CNSecond Military Medical University · CNFudan University · CNTianjin Medical University Cancer Institute and Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveRecent researches have demonstrated that inflammation-related diseases are effectively regulated by posttranslational modifications (PTMs) including phosphorylation and acetylation. Our previous study found a new acetyltransferase inhibitor, oridonin, which had a protective effect on acute liver injury (ALI). In the present study, we further investigated its protective mechanism against D-galactosamine (D-Gal) combined with lipopolysaccharide- (LPS-) induced ALI in mice.

methodsIntraperitoneal injections of LPS (40

resultsGO analysis showed that genes that were downregulated after pretreatment with oridonin were extremely concentrated in immune response, chemotaxis, and inflammatory response. Real-time PCR confirmed that the expression of these genes was upregulated by LPS/D-Gal induction and reduced after treatment with oridonin, which was consistent with RNA-Seq results. KEGG pathway analysis showed a significantly enriched downregulated gene that was present in the Toll-like receptor (TLR) 4 signaling cascade. Our results manifested that phosphorylation levels of upstream signaling molecules in the TLR4 signaling cascade, including extracellular signal-regulated kinase (ERK), P38, and I

conclusionOur study revealed that the protective effects of oridonin on LPS/D-Gal-induced ALI mediated by inhibition of the PTMs of IRAK4, including phosphorylation of T345/S346 and acetylation of K34.

Indexed as

AcetylationAnimalsChemical and Drug Induced Liver InjuryDiterpenes, KauraneFemaleInterleukin-1 Receptor-Associated KinasesLipopolysaccharidesMiceMice, Inbred C57BLProtein Processing, Post-TranslationalToll-Like Receptor 4Diterpenes, KauraneInterleukin-1 Receptor-Associated KinasesIrak4 protein, mouseLipopolysaccharidesoridoninToll-Like Receptor 4

Identifiers

PMID31611735
PMCPMC6757283
OpenAlexW2972787006

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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.