Evidence map›Paper›PMID 30568428›Full record

ArticleDrug design, development and therapy2018

Beraprost sodium preconditioning prevents inflammation, apoptosis, and autophagy during hepatic ischemia-reperfusion injury in mice via the P38 and JNK pathways.

Jingfan Deng, Jiao Feng, Tong Liu, Xiya Lu, Wenwen Wang, Ning Liu, Yang Lv, Qing Liu, Chuanyong Guo, Yingqun Zhou

Open access · goldAbstract read
In one paragraph

Article in Drug design, development and therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

22 citing papers in PubMed, 36 citations in OpenAlex.

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  12. Treprostinil alleviates hepatic mitochondrial injury during rat renal ischemia-reperfusion injury.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2021
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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 2 countries.

Jingfan DengDepartment of Gastroenterology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai 200072, People's Republic of China, guochuanyong@hotmail.com; yqzh02@163.com.
Jiao FengDepartment of Gastroenterology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai 200072, People's Republic of China, guochuanyong@hotmail.com; yqzh02@163.com.
Tong LiuDepartment of Gastroenterology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai 200072, People's Republic of China, guochuanyong@hotmail.com; yqzh02@163.com.
Xiya LuDepartment of Gastroenterology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai 200072, People's Republic of China, guochuanyong@hotmail.com; yqzh02@163.com.
Wenwen WangDepartment of Gastroenterology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai 200072, People's Republic of China, guochuanyong@hotmail.com; yqzh02@163.com.
Ning LiuDepartment of Gastroenterology, Shanghai Tenth People's Hospital, School of Clinical Medicine of Nanjing Medical University, Shanghai 200072, People's Republic of China.
Yang LvDepartment of Gastroenterology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai 200072, People's Republic of China, guochuanyong@hotmail.com; yqzh02@163.com.
Qing LiuDepartment of Gastroenterology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai 200072, People's Republic of China, guochuanyong@hotmail.com; yqzh02@163.com.
Chuanyong GuoDepartment of Gastroenterology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai 200072, People's Republic of China, guochuanyong@hotmail.com; yqzh02@163.com.
Yingqun ZhouDepartment of Gastroenterology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai 200072, People's Republic of China, guochuanyong@hotmail.com; yqzh02@163.com.
University Gastroenterology · USShanghai Tenth People's Hospital · CNTongji University · CNNanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveThe goal of this study was to determine the effects of beraprost sodium (BPS) preconditioning on hepatic ischemia-reperfusion (IR) injury and its underlying mechanisms of action. MATERIALS AND

methodsMice were randomly divided into sham, IR, IR+BPS (50 µg/kg), and IR+BPS (100 µg/kg) groups. Saline or BPS was given to the mice by daily gavage for 1 week before the hepatic IR model was established. Liver tissues and orbital blood were collected at 2, 8, and 24 hours after reperfusion for the determination of liver enzymes, inflammatory mediators, apoptosis- and autophagy-related proteins, key proteins in P38 and c-Jun N-terminal kinase (JNK) cascades, and evaluation of liver histopathology.

resultsBPS preconditioning effectively reduced serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels, improved pathological damage, ameliorated production of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β), and affected expressions of Bax, Bcl-2, Caspase-3, Caspase-8, and Caspase-9, microtubule-associated protein 1 light chain 3 (LC3), Beclin-1, and P62. The protective effects of BPS preconditioning were associated with reduced P38 and JNK phosphorylation.

conclusionBPS preconditioning ameliorated hepatic IR injury by suppressing inflammation, apoptosis, and autophagy, partially via inhibiting activation of the P38 and JNK cascades.

Indexed as

AnimalsAnti-Inflammatory AgentsApoptosisApoptosis Regulatory ProteinsAutophagyAutophagy-Related ProteinsCytoprotectionDisease Models, AnimalDrug Administration ScheduleEpoprostenolHepatitisInflammation MediatorsJNK Mitogen-Activated Protein KinasesLiverMaleMice, Inbred BALB CAnti-Inflammatory AgentsApoptosis Regulatory ProteinsAutophagy-Related ProteinsberaprostEpoprostenolInflammation MediatorsJNK Mitogen-Activated Protein Kinasesp38 Mitogen-Activated Protein Kinasesapoptosisautophagyberaprost sodiuminflammationliver injuryMAPK pathway

Identifiers

PMID30568428
PMCPMC6276616
OpenAlexW2902214750

What OpenQuestion holds

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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.