Evidence map›Paper›PMID 35233372›Full record

ArticleJournal of clinical and translational hepatology2022

Hepatic Ischemia-reperfusion Injury in Mice was Alleviated by Rac1 Inhibition - More Than Just ROS-inhibition.

Zhilin Sha, Yajie Yang, Ruling Liu, Haili Bao, Shaohua Song, Junfeng Dong, Meng Guo, Yuanyu Zhao, Hu Liu, Guoshan Ding

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

Article in Journal of clinical and translational hepatology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

7 citing papers in PubMed, 11 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

10 authors at 2 institutions in 1 country.

Zhilin ShaDepartment of Organ Transplantation, Second Affiliated Hospital of Naval Medical University, Shanghai, China.
Yajie YangCollege of Basic Medicine, Naval Medical University, Shanghai, China.
Ruling LiuDepartment of Radiation Medicine, Faculty of Naval Medicine, Naval Medical University, Shanghai, China.
Haili BaoDepartment of Organ Transplantation, Second Affiliated Hospital of Naval Medical University, Shanghai, China.
Shaohua SongDepartment of General Surgery, Ruijin Hospital, Shanghai Jiao Tong University, School of Medicine, Shanghai, China.
Junfeng DongDepartment of Organ Transplantation, Second Affiliated Hospital of Naval Medical University, Shanghai, China.
Meng GuoDepartment of Organ Transplantation, Second Affiliated Hospital of Naval Medical University, Shanghai, China.
Yuanyu ZhaoDepartment of Organ Transplantation, Second Affiliated Hospital of Naval Medical University, Shanghai, China.
Hu LiuDepartment of Radiation Medicine, Faculty of Naval Medicine, Naval Medical University, Shanghai, China.
Guoshan DingDepartment of Organ Transplantation, Second Affiliated Hospital of Naval Medical University, Shanghai, China.ORCID https://orcid.org/0000-0001-8127-1053
Second Military Medical University · CNShanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

aimsReducing reactive oxygen species (ROS) production has proven an effective way for alleviating oxidative stress during ischemia-reperfusion injury (IRI). Moreover, inhibition of Rac1 could reduce ROS production and prevent oxidative stress injury. Previous studies have suggested a positive interactivation feedback loop between Rac1 and hypoxia-inducible factor (HIF)-1α, the latter being up-regulated early during ischemia. The positive inter-activation between Rac1 and HIF-1α would aggravate ROS production, thereby promoting IRI. This study was designed to verify the effects of Rac1 inhibition on hepatic IRI both at animal and cellular levels and to explore the interaction between Rac1 and HIF-1α during hepatic IRI.

methodsC57B/6 mice and AML-12 cells were used for the construction of hepatic IRI animal and cell models. Rac1 inhibition was achieved by NSC23766 (a specific Rac1 inhibitor). Lentiviral vectors were used for Rac1 knockdown. At designated time points, serum and liver tissues were collected from the mice and treated cells were collected for further analysis.

resultsNSC23766 treatment significantly alleviated the hepatic IRI in mice, manifesting as lower vacuolation score and less apoptosis cells, lower ROS and serum/liver alanine aminotransferase/aspartate aminotransferase levels, and fewer activated inflammatory cells. IRI of AML-12 was also alleviated by 50 µM NSC23766 or Rac1-knockdown, manifesting as reduced cell apoptosis, less extensive interruption of mitochondrial membrane potential, down-regulation of apoptosis, and effects on DNA damage-related proteins. Interestingly, Rac1 knockdown also down-regulated the expression level of HIF-1α.

conclusionsOur study supports a protective effect of Rac1 inhibition on hepatic IRI. Aside from the classic topics of reducing ROS production and oxidative stress, our study showed an interaction between Rac1 and HIF-1α signaling during hepatic IRI.

Indexed as

Hepatic ischemia-reperfusion injuryHypoxia inducible factorRac1Reactive oxygen species

Identifiers

PMID35233372
PMCPMC8845157
OpenAlexW3180413158

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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.