Evidence map›Paper›PMID 37353787›Full record

ArticleBMC complementary medicine and therapies2023

2-phenylacetamide Separated from the seed of Lepidium apetalum Willd. inhibited renal fibrosis via MAPK pathway mediated RAAS and oxidative stress in SHR Rats.

Pei-Pei Yuan, Meng Li, Qi Zhang, Meng-Nan Zeng, Ying-Ying Ke, Ya-Xin Wei, Yang Fu, Xiao-Ke Zheng, Wei-Sheng Feng

Open access · goldAbstract read
In one paragraph

Article in BMC complementary medicine and therapies, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 14% 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

5 citing papers in PubMed, 1 synthesis or guideline pooled it, 8 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

9 authors at 2 institutions in 1 country.

Pei-Pei YuanCollege of Pharmacy, Henan University of Chinese Medicine, Zhengzhou, 450046, China.
Meng LiCollege of Pharmacy, Henan University of Chinese Medicine, Zhengzhou, 450046, China.
Qi ZhangCollege of Pharmacy, Henan University of Chinese Medicine, Zhengzhou, 450046, China.
Meng-Nan ZengCollege of Pharmacy, Henan University of Chinese Medicine, Zhengzhou, 450046, China.
Ying-Ying KeCollege of Pharmacy, Henan University of Chinese Medicine, Zhengzhou, 450046, China.
Ya-Xin WeiCollege of Pharmacy, Henan University of Chinese Medicine, Zhengzhou, 450046, China.
Yang FuCollege of Pharmacy, Henan University of Chinese Medicine, Zhengzhou, 450046, China.
Xiao-Ke ZhengCollege of Pharmacy, Henan University of Chinese Medicine, Zhengzhou, 450046, China. zhengxk.2006@163.com.
Wei-Sheng FengCollege of Pharmacy, Henan University of Chinese Medicine, Zhengzhou, 450046, China. fwsh@hactcm.edu.cn.
First Affiliated Hospital of Henan University · CNHenan Bioengineering Technology Research Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundRenal fibrosis with Renin-angiotensin-aldosterone system (RAAS) activation and oxidative stress are one of the major complications in hypertension. 2-phenylacetamide (PA), a major active component of Lepidium apetalum Willd. (L.A), has numerous pharmacological effects. Its analogues have the effect of anti-renal fibrosis and alleviating renal injury. This study aims to explore the underlying mechanism of PA for regulating the renal fibrosis in SHR based on the MAPK pathway mediated RAAS and oxidative stress.

methodsThe SHR rats were used as the hypertension model, and the WKY rats were used as the control group. The blood pressure (BP), urine volume were detected every week. After PA treatment for 4 weeks, the levels of RAAS, inflammation and cytokines were measured by Enzyme-Linked Immunosorbnent Assay (ELISA). Hematoxylin-Eosin staining (HE), Masson and Immunohistochemistry (IHC) were used to observe the renal pathology, collagen deposition and fibrosis. Western blot was used to examine the MAPK pathway in renal. Finally, the SB203580 (p38 MAPK inhibitor) antagonism assay in the high NaCl-induced NRK52e cells was used, together with In-Cell Western (ICW), Flow Cytometry (FCM), High Content Screening (HCS) and ELISA to confirm the potential pharmacological mechanism.

resultsPA reduced the BP, RAAS, inflammation and cytokines, promoted the urine, and relieved renal pathological injury and collagen deposition, repaired renal fibrosis, decreased the expression of NADPH Oxidase 4 (NOX4), transforming growth factor-β (TGF-β), SMAD3 and MAPK signaling pathway in SHR rats. Meanwhile,,the role of PA could be blocked by p38 antagonist SB203580 effectively in the high NaCl-induced NRK52e cells. Moreover, molecular docking indicated that PA occupied the ligand binding sites of p38 MAPK.

conclusionPA inhibited renal fibrosis via MAPK signalling pathway mediated RAAS and oxidative stress in SHR Rats.

Indexed as

BenzeneacetamidesHypertensionKidney DiseasesLepidiumAnimalsCollagenCytokinesFibrosisInflammationMolecular Docking SimulationOxidative Stressp38 Mitogen-Activated Protein KinasesRatsRats, Inbred SHRRats, Inbred WKYRenin-Angiotensin SystemBenzeneacetamidesCollagenCytokinesp38 Mitogen-Activated Protein KinasesSodium Chloride2-phenylacetamideHypertensionLepidium apetalum Willd.MAPK signalling pathwayOxidative stressRAASRenal fibrosis

Identifiers

PMID37353787
PMCPMC10290354
OpenAlexW4381839651

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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.