Evidence map›Paper›PMID 35428330›Full record

ArticleBMC pharmacology & toxicology2022

ROCK inhibitor fasudil reduces the expression of inflammatory factors in LPS-induced rat pulmonary microvascular endothelial cells via ROS/NF-κB pathway.

Huanlong Liu, Zhenhua Pan, Xindi Ma, Junru Cui, Juan Gao, Qingfeng Miao, Zhongning Zhu, Xueyan Chen, Suwen Su

Open access · goldAbstract read
In one paragraph

Article in BMC pharmacology & toxicology, 2022. 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
3.5field-weighted citation impact, top 8% 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, 30 citations in OpenAlex.

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  7. Anti-Inflammatory Effect of 21Food science & nutrition · 2025
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  8. NF-κB and pulmonary hypertension: Advances in mechanistic research and therapeutic applications.American heart journal plus : cardiology research and practice · 2025
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  16. Chemical Constituents from the Fruit ofAntioxidants (Basel, Switzerland) · 2024
    Article
  17. Article
  18. Article
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  20. Review
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

9 authors at 2 institutions in 1 country.

Huanlong LiuPharmaceutical Department of the Second Hospital of Hebei Medical University, Shijiazhuang, PR China.
Zhenhua PanDepartment of Pharmacy, Hebei Medical University, Shijiazhuang, PR China.
Xindi MaDepartment of Pharmacology, Hebei Medical University, The Key Laboratory of Neural and Vascular Biology, Ministry of Education, The Key Laboratory of Pharmacology and Toxicology for New Drugs, 361 East Zhongshan Road, Shijiazhuang, 050017, PR China.
Junru CuiDepartment of Pharmacology, Hebei Medical University, The Key Laboratory of Neural and Vascular Biology, Ministry of Education, The Key Laboratory of Pharmacology and Toxicology for New Drugs, 361 East Zhongshan Road, Shijiazhuang, 050017, PR China.
Juan GaoPharmaceutical Department of the Second Hospital of Hebei Medical University, Shijiazhuang, PR China.
Qingfeng MiaoDepartment of Pharmacology, Hebei Medical University, The Key Laboratory of Neural and Vascular Biology, Ministry of Education, The Key Laboratory of Pharmacology and Toxicology for New Drugs, 361 East Zhongshan Road, Shijiazhuang, 050017, PR China.
Zhongning ZhuDepartment of Pharmacology, Hebei Medical University, The Key Laboratory of Neural and Vascular Biology, Ministry of Education, The Key Laboratory of Pharmacology and Toxicology for New Drugs, 361 East Zhongshan Road, Shijiazhuang, 050017, PR China.
Xueyan ChenDepartment of Pharmacology, Hebei Medical University, The Key Laboratory of Neural and Vascular Biology, Ministry of Education, The Key Laboratory of Pharmacology and Toxicology for New Drugs, 361 East Zhongshan Road, Shijiazhuang, 050017, PR China. cxylong@126.com.
Suwen SuDepartment of Pharmacology, Hebei Medical University, The Key Laboratory of Neural and Vascular Biology, Ministry of Education, The Key Laboratory of Pharmacology and Toxicology for New Drugs, 361 East Zhongshan Road, Shijiazhuang, 050017, PR China. suswmk@163.com.
Hebei Medical University · CNSecond Hospital of Hebei Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundInflammation plays a major role in the pulmonary artery hypertension (PAH) and the acute lung injury (ALI) diseases. The common feature of these complications is the dysfunction of pulmonary microvascular endothelial cells (PMVECs). Fasudil, the only Rho kinase (ROCK) inhibitor used in clinic, has been proved to be the most promising new drug for the treatment of PAH, with some anti-inflammatory activity. Therefore, in the present study, the effect of fasudil on lipopolysaccharide (LPS)-induced inflammatory injury in rat PMVECs was investigated.

methodsLPS was used to make inflammatory injury model of rat PMVECs. Thereafter, the mRNA and protein expression of pro-inflammatory factors was evaluated by reverse transcription-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA) assay respectively. Intracellular reactive oxygen species (ROS) levels were measured by the confocal laser scanning system. The activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and the content of malondialdehyde (MDA) were determined by using commercial kits according to the manufacturer's instructions. Western blot assay was used to detect the protein expression of nuclear factor kappa B (NF-κB) p65.

resultsFasudil effectively prevented inflammatory injury induced by LPS, which is manifested by the decrease of pro-inflammatory cytokines interleukin-6 (IL-6) and monocyte chenotactic protein-1 (MCP-1). Meanwhile, fasudil dramatically reduced the levels of ROS and MDA, and also elevated the activities of SOD and GSH-Px. Furthermore, the nuclear translocation of NF-κB p65 induced by LPS was also suppressed by fasudil. Additionally, the ROS scavengers N-Acetylcysteine (N-Ace) was also found to inhibit the nuclear translocation of NF-κB and the mRNA expression of IL-6 and MCP-1 induced by LPS, which suggested that ROS was essential for the nuclear translocation of NF-κB.

conclusionsThe present study revealed that fasudil reduced the expression of inflammatory factors, alleviated the inflammatory and oxidative damage induced by LPS in rat PMVECs via ROS-NF-κB signaling pathway.

Indexed as

LipopolysaccharidesNF-kappa B1-(5-Isoquinolinesulfonyl)-2-MethylpiperazineAnimalsEndothelial CellsInterleukin-6Protein Kinase InhibitorsRatsReactive Oxygen Speciesrho-Associated KinasesRNA, MessengerSuperoxide Dismutase1-(5-Isoquinolinesulfonyl)-2-MethylpiperazinefasudilInterleukin-6LipopolysaccharidesNF-kappa BProtein Kinase InhibitorsReactive Oxygen Speciesrho-Associated KinasesRNA, MessengerSuperoxide DismutaseFasudilInflammationLipopolysaccharideNF-κBPulmonary microvascular endothelial cellsROS

Identifiers

PMID35428330
PMCPMC9013060
OpenAlexW4224072529

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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.