Evidence map›Paper›PMID 32231583›Full record

ArticleFrontiers in physiology2020

Pharmacologic Blockade of 15-PGDH Protects Against Acute Renal Injury Induced by LPS in Mice.

Shuying Miao, Caihong Lv, Ying Liu, Jie Zhao, Ting Li, Chunjiang Wang, Yunfei Xu, Xiaoli Wang, Xianzhong Xiao, Huali Zhang

Open access · goldAbstract read
In one paragraph

Article in Frontiers in physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

20 citing papers in PubMed, 32 citations in OpenAlex.

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  11. Ginsenoside Rb1 Promotes Hepatic Glycogen Synthesis to Ameliorate T2DM Through 15-PGDH/PGEDiabetes, metabolic syndrome and obesity : targets and therapy · 2023
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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

10 authors at 4 institutions in 1 country.

Shuying MiaoDepartment of Pathophysiology, Xiangya School of Medicine, Central South University, Changsha, China.
Caihong LvDepartment of Pathophysiology, Xiangya School of Medicine, Central South University, Changsha, China.
Ying LiuDepartment of Pathophysiology, Xiangya School of Medicine, Central South University, Changsha, China.
Jie ZhaoDepartment of Neurosurgery, Xiangya Hospital, Central South University, Changsha, China.
Ting LiDepartment of Physiology, Changzhi Medical College, Changzhi, China.
Chunjiang WangDepartment of Pharmacy, The Third Xiangya Hospital, Central South University, Changsha, China.
Yunfei XuDepartment of Pathophysiology, Xiangya School of Medicine, Central South University, Changsha, China.
Xiaoli WangDepartment of Pathology and Pathophysiology, Jishou University, Jishou, China.
Xianzhong XiaoDepartment of Pathophysiology, Xiangya School of Medicine, Central South University, Changsha, China.
Huali ZhangDepartment of Pathophysiology, Xiangya School of Medicine, Central South University, Changsha, China.
Central South University · CNChangzhi Medical College · CNJishou University · CNThird Xiangya Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prostaglandin pathway plays multiple roles in various physiological and pathological conditions. The present study aimed to investigate the effect of 15-hydroxyprostaglandin dehydrogenase (15-PGDH), a key enzyme in the degradation of prostaglandins, on lipopolysaccharide (LPS)-induced acute kidney injury (AKI) in mice. In this study, male C57BL/6J mice were injected intraperitoneally with LPS (10 mg/kg). SW033291, a potent small-molecule inhibitor of 15-PGDH, was used to investigate the therapeutic potential of 15-PGDH inhibition on LPS-induced AKI. We discovered that the expression of 15-PGDH protein was upregulated in kidneys of LPS-stimulated mice, and it was mainly localized in the cytoplasm of renal tubular epithelial cells in renal cortex and outer medulla. SW033291 administration improved the survival rates of mice and attenuated renal injury of mice that were challenged by LPS. Additionally, inhibition of 15-PGDH also reversed LPS-induced apoptosis of renal cells, increased expression of anti-apoptotic protein Bcl-2, and downregulated expression of Fas, caspase-3, and caspase-8. Pretreatment of SW033291 enhanced autophagy in kidney cells after LPS stimulation. Our data also showed that inhibition of 15-PGDH relieved the level of lipid peroxidation and downregulated NADPH oxidase subunits induced by LPS in mice kidneys but had no significant effect on the release of inflammatory factors, such as IL-6, IL-1β, TNF-α, and MCP-1. Our study demonstrated that inhibition of 15-PGDH could alleviate LPS-induced AKI by regulating the apoptosis, autophagy, and oxidative stress rather than inflammation in mice.

Indexed as

15-PGDHAKIapoptosisautophagyLPSoxidative stress

Identifiers

PMID32231583
PMCPMC7082810
OpenAlexW3010795190

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Registered trials

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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.