Evidence map›Paper›PMID 36938407›Full record

ArticleHeliyon2023

Embelin attenuates lipopolysaccharide-induced acute kidney injury through the inhibition of M1 macrophage activation and NF-κB signaling in mice.

Qiao Tang, Yun Tang, Qun Yang, Rong Chen, Hong Zhang, Haojun Luo, Qiong Xiao, Kaixiang Liu, Liming Huang, Jie Chen and 6 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Heliyon, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.9field-weighted citation impact, top 10% 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

11 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
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

16 authors at 2 institutions in 1 country.

Qiao TangNorth Sichuan Medical College, Nanchong, 637000, Sichuan, China.
Yun TangDepartment of Nephrology, Sichuan Provincial People's Hospital, Sichuan Clinical Research Center for Kidney Diseases, University of Electronic Science and Technology of China, Chengdu, 610072, Sichuan, China.
Qun YangDepartment of Pathology, School of Medicine, Sichuan Academy of Medical Science and Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, 610072, Sichuan, China.
Rong ChenDepartment of Nephrology, Sichuan Provincial People's Hospital, Sichuan Clinical Research Center for Kidney Diseases, University of Electronic Science and Technology of China, Chengdu, 610072, Sichuan, China.
Hong ZhangDepartment of Nephrology, Sichuan Provincial People's Hospital, Sichuan Clinical Research Center for Kidney Diseases, University of Electronic Science and Technology of China, Chengdu, 610072, Sichuan, China.
Haojun LuoDepartment of Nephrology, Sichuan Provincial People's Hospital, Sichuan Clinical Research Center for Kidney Diseases, University of Electronic Science and Technology of China, Chengdu, 610072, Sichuan, China.
Qiong XiaoDepartment of Nephrology, Sichuan Provincial People's Hospital, Sichuan Clinical Research Center for Kidney Diseases, University of Electronic Science and Technology of China, Chengdu, 610072, Sichuan, China.
Kaixiang LiuDepartment of Nephrology, Sichuan Provincial People's Hospital, Sichuan Clinical Research Center for Kidney Diseases, University of Electronic Science and Technology of China, Chengdu, 610072, Sichuan, China.
Liming HuangDepartment of Nephrology, Sichuan Provincial People's Hospital, Sichuan Clinical Research Center for Kidney Diseases, University of Electronic Science and Technology of China, Chengdu, 610072, Sichuan, China.
Jie ChenCentral Laboratory, Sichuan Academy of Medical Science and Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, 610072, Sichuan, China.
Lin WangInstitute of Laboratory Animal Sciences, School of Medicine, Sichuan Academy of Medical Science and Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, 610072, Sichuan, China.
Xinrou SongDepartment of Nephrology, Sichuan Provincial People's Hospital, Sichuan Clinical Research Center for Kidney Diseases, University of Electronic Science and Technology of China, Chengdu, 610072, Sichuan, China.
Sipei ChenDepartment of Nephrology, Sichuan Provincial People's Hospital, Sichuan Clinical Research Center for Kidney Diseases, University of Electronic Science and Technology of China, Chengdu, 610072, Sichuan, China.
Guisen LiDepartment of Nephrology, Sichuan Provincial People's Hospital, Sichuan Clinical Research Center for Kidney Diseases, University of Electronic Science and Technology of China, Chengdu, 610072, Sichuan, China.
Li WangDepartment of Nephrology, Sichuan Provincial People's Hospital, Sichuan Clinical Research Center for Kidney Diseases, University of Electronic Science and Technology of China, Chengdu, 610072, Sichuan, China.
Yi LiDepartment of Nephrology, Sichuan Provincial People's Hospital, Sichuan Clinical Research Center for Kidney Diseases, University of Electronic Science and Technology of China, Chengdu, 610072, Sichuan, China.
University of Electronic Science and Technology of China · CNNorth Sichuan Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Septic acute kidney injury (AKI) is commonly associated with renal dysfunction and high mortality in patients. Owing to the rapid and violent occurrence of septic AKI with inflammation, there are no effective therapies to clinically treat it. Embelin, a natural product, has a potential regulatory role in immunocytes. However, the role and mechanism of embelin in septic AKI remains unknown. This study aimed to elucidate the role of embelin in macrophage regulation in lipopolysaccharide (LPS)-induced septic AKI. Embelin was intraperitoneally administered to mice after LPS injection. And bone marrow-derived macrophages (BMDMs) were subsequently isolated from the mice to explore the immunomodulatory role of embelin in macrophages. We found that embelin attenuated renal dysfunction and pathological renal damage in the LPS-induced sepsis mouse model. Molecular docking predicted that embelin could bind to phosphorylated NF-κB p65 at the ser536 site. Embelin inhibited the translocation of NF-κB p65 via phosphorylation at ser536 in LPS-induced AKI. It also reduced the secretion of IL-1β and IL-6 and increased the secretion of IL-10 and Arg-1 of BMDMs and mice after LPS stimulation, indicating that embelin suppressed macrophage M1 activation in LPS-induced AKI. Therefore, embelin attenuated LPS-induced septic AKI by suppressing NF-κB p65 at ser536 in activated macrophages. This study preclinically suggests a therapeutic role of embelin in septic AKI.

Indexed as

AKI, acute kidney injuryBMDMs, bone marrow-derived macrophagesBUN, blood urea nitrogenDMEM, Dulbecco's modified eagle's mediumEmbelinFBS, fetal bovine serumHE, hematoxylin & eosinICU, intensive care unitIHC, immunohistochemistryInflammationLPS, lipopolysaccharideMacrophagemIF, multiplex immunofluorescentPAS, periodic-acid SchiffPhosphorylated NF-κB p65 translocationScr, serum creatinineSeptic acute kidney injury

Identifiers

PMID36938407
PMCPMC10018479
OpenAlexW4322102199

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.