Evidence map›Paper›PMID 35092471›Full record

ArticleNaunyn-Schmiedeberg's archives of pharmacology2022

Ferulic acid prevents cyclosporine-induced nephrotoxicity in rats through exerting anti-oxidant and anti-inflammatory effects via activation of Nrf2/HO-1 signaling and suppression of NF-κB/TNF-α axis.

Ali Nouri, Keihan Ghatreh-Samani, Hossein Amini-Khoei, Asghar Mohammadi, Esfandiar Heidarian, Mohammad Najafi

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In one paragraph

Article in Naunyn-Schmiedeberg's archives of pharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
5.2field-weighted citation impact, top 4% 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

16 citing papers in PubMed, 26 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

6 authors at 2 institutions in 1 country.

Ali NouriDepartment of Biochemistry, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Keihan Ghatreh-SamaniClinical Biochemistry Research Center, Basic Health Sciences Institute, Shahrekord University of Medical Sciences, Shahrekord, Iran.
Hossein Amini-KhoeiMedical Plant Research Center, Basic Health Sciences Institute, Shahrekord University of Medical Sciences, Shahrekord, Iran.
Asghar MohammadiDepartment of Biochemistry, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Esfandiar Heidarian *Clinical Biochemistry Research Center, Basic Health Sciences Institute, Shahrekord University of Medical Sciences, Shahrekord, Iran. heidarian46@yahoo.com.
Mohammad Najafi *Department of Biochemistry, School of Medicine, Iran University of Medical Sciences, Tehran, Iran. nbsmmsbn@iums.ac.ir.ORCID 0000-0002-0622-4174
Iran University of Medical Sciences · IRShahrekord University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cyclosporine is one of the main immunosuppressive agents used in the treatment of autoimmune diseases or transplantation. Despite the favorable effects, cyclosporine-mediated nephrotoxicity critically restricts the clinical use of the agent. Given this, herein, we aimed to evaluate whether ferulic acid could prevent cyclosporine-mediated nephrotoxicity in rats. A total of 32 Wistar rats were chosen to be treated with cyclosporine, ferulic acid, and the combination of both agents for 21 days. To evaluate the nephron-protective mechanism of ferulic acid, the serum levels of biochemical parameters, as well as the tissue levels of several oxidative and anti-oxidative mediators, were examined. The expression and the tissue levels of nuclear factor (NF)-κB, tumor necrosis factor (TNF)-α, heme oxygenase (HO-1), and nuclear factor erythroid 2-related factor 2 (Nrf2) were evaluated using the qRT-PCR and ELISA, respectively. Our results showed while cyclosporine elevated the serum levels of renal-related markers in the rats, in the presence of ferulic acid, there was a significant reduction in the levels of urea, uric acid, creatinine, and sGOT. Moreover, we found that ferulic acid remarkably prevented cyclosporine-mediated nephrotoxicity by restoring the anti-oxidant system through activating the Nrf2/HO-1 axis. By halting the NF-κB-mediated upregulation of TNF-α, it also seems that ferulic acid prevented lymphocytes infiltration into kidney tissue and consequently suppressed inflammatory responses. Overall, the results of the present study suggest that due to the anti-oxidant and anti-inflammatory properties of ferulic acid, this agent could be used alongside cyclosporine to reduce its adverse effects on kidney tissue.

Indexed as

NF-E2-Related Factor 2NF-kappa BAnimalsAnti-Inflammatory AgentsAntioxidantsCoumaric AcidsCyclosporineHeme Oxygenase-1KidneyOxidative StressRatsRats, WistarTumor Necrosis Factor-alphaAnti-Inflammatory AgentsAntioxidantsCoumaric AcidsCyclosporineferulic acidHeme Oxygenase-1NF-E2-Related Factor 2NF-kappa BTumor Necrosis Factor-alphaAnti-inflammatory responsesAnti-oxidant systemCyclosporineFerulic acidNephrotoxicity

Identifiers

PMID35092471
OpenAlexW4210664977

What OpenQuestion holds

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Read underepoch 390

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.