Evidence map›Paper›PMID 31105861›Full record

ArticleAmerican journal of translational research2019

Effect of splenectomy on attenuation of LPS-induced AKI through GTS-21-induced cholinergic anti-inflammatory pathway.

Yang Gao, Kai Kang, Xinyu Zhang, Qiuyuan Han, Haitao Liu, Weilan Kong, Xing Zhang, Rui Huang, Zhenyu Yang, Zhidong Qi and 9 more

Open access · greenAbstract read
In one paragraph

Article in American journal of translational research, 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 30% 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, 13 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

19 authors at 2 institutions in 1 country.

Yang GaoDepartment of Critical Care Medicine, The Second Affiliated Hospital of Harbin Medical University Harbin 150086, China.
Kai KangDepartment of Critical Care Medicine, The First Affiliated Hospital of Harbin Medical University Harbin 150001, China.
Xinyu ZhangDepartment of Critical Care Medicine, The First Affiliated Hospital of Harbin Medical University Harbin 150001, China.
Qiuyuan HanDepartment of Critical Care Medicine, The Second Affiliated Hospital of Harbin Medical University Harbin 150086, China.
Haitao LiuDepartment of Critical Care Medicine, The Cancer Hospital of Harbin Medical University Harbin 150081, China.
Weilan KongDepartment of Critical Care Medicine, The First Affiliated Hospital of Harbin Medical University Harbin 150001, China.
Xing ZhangDepartment of Critical Care Medicine, The Second Affiliated Hospital of Harbin Medical University Harbin 150086, China.
Rui HuangDepartment of Critical Care Medicine, The Second Affiliated Hospital of Harbin Medical University Harbin 150086, China.
Zhenyu YangDepartment of Critical Care Medicine, The Second Affiliated Hospital of Harbin Medical University Harbin 150086, China.
Zhidong QiDepartment of Critical Care Medicine, The Second Affiliated Hospital of Harbin Medical University Harbin 150086, China.
Junbo ZhengDepartment of Critical Care Medicine, The Second Affiliated Hospital of Harbin Medical University Harbin 150086, China.
Ming LiDepartment of Critical Care Medicine, The Second Affiliated Hospital of Harbin Medical University Harbin 150086, China.
Jiayu LiDepartment of Critical Care Medicine, The Cancer Hospital of Harbin Medical University Harbin 150081, China.
Ruijin LiuDepartment of Critical Care Medicine, The Cancer Hospital of Harbin Medical University Harbin 150081, China.
Yansong LiuDepartment of Critical Care Medicine, The Cancer Hospital of Harbin Medical University Harbin 150081, China.
Sicong WangDepartment of Critical Care Medicine, The Cancer Hospital of Harbin Medical University Harbin 150081, China.
Weihua ZhangDepartment of Pathophysiology, Harbin Medical University Harbin 150086, China.
Hongliang WangDepartment of Critical Care Medicine, The Second Affiliated Hospital of Harbin Medical University Harbin 150086, China.
Kaijiang YuDepartment of Critical Care Medicine, The First Affiliated Hospital of Harbin Medical University Harbin 150001, China.
Harbin Medical University · CNHarbin Engineering University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This work was undertaken to explore the role of splenectomy on attenuation of lipopolysaccharide (LPS)-induced acute kidney injury (AKI) through GTS-21-induced cholinergic anti-inflammatory pathway. C57BL/6 mice were used to construct models of sepsis-induced renal injury. HE, Tunel and blood assays were used to determine the success of the model. The animals were examined after splenectomy with or without LPS and GTS-21+LPS treatments. The pathological changes and apoptosis in the renal tissue were detected using HE and Tunel assays. The contents of creatinine (Cr) and cystatin-C (Cys-C) were measured using ELISA. The expression of IL-6, NF-kB p65, Caspase-3, anti-apoptotic protein Bcl-2, apoptotic protein Bax and α7nAChR was quantified using qRT-PCR. The expression of Bcl-2, Bax, Caspase-3, IL-6, NF-kB p65, α7nAChR and p-STAT3 was using assessed using Western blot analysis. HE, Tunel, BUN and serum creatinine (SC) assay showed that renal injury models were successfully established. Compared with the control, the apoptosis in the LPS group was significantly increased and decreased after GTS-21 treatment. However, splenectomy combined with GTS-21 increased the apoptosis, indicating that splenectomy could partially offset the anti-apoptosis effect of GTS-21. In animals treated with LPS, the contents of Cr and Cys-C increased significantly. These contents reduced following GTS-21 treatment, but increased after splenectomy. After LPS treatment, the expression of IL-6, NF-kB p65, p-STAT3, Caspase-3 and Bax was significantly up-regulated, while the expression of α7nAChR and Bcl-2 significantly down-regulated. Compared with LPS treated mice, splenectomy reduced the expression of IL-6, NF-kB p65 and p-STAT3, suggesting that splenectomy inhibits the activation of α7nAChR pathway by the GTS-21. It is clear that GTS-21 effectively attenuates LPS-induced renal injury; splenectomy suppresses the anti-inflammatory and anti-apoptosis activity and renal protective effect of GTS-21. On other hand, splenectomy reduces the production of inflammatory cytokines in the circulation, and has certain protective effect on the kidney. Therefore, the impact of splenectomy on LPS-induced AKI depends on the strength of the two aspects.

Indexed as

AKIapoptosischolinergic anti-inflammatory pathwayGTS-21inflammatory reactionLPSSplenectomy

Identifiers

PMID31105861
PMCPMC6511767
OpenAlexW2982891252

What OpenQuestion holds

Textmetadata
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.