Evidence map›Paper›PMID 35764864›Full record

ArticleInflammopharmacology2022

Targeting inflammation and redox perturbations by lisinopril mitigates Freund's adjuvant-induced arthritis in rats: role of JAK-2/STAT-3/RANKL axis, MMPs, and VEGF.

Hany H Arab, Sarah A Abd El-Aal, Ahmed M Ashour, Azza A K El-Sheikh, Hana J Al Khabbaz, El-Shaimaa A Arafa, Ayman M Mahmoud, Ahmed M Kabel

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In one paragraph

Article in Inflammopharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

13 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Mechanistic Study of Yibi Decoction in Treating Rheumatoid ArthritisEndocrine, metabolic & immune disorders drug targets · 2026
    Article
  5. Article
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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

8 authors at 8 institutions in 5 countries.

Hany H ArabDepartment of Pharmacology and Toxicology, College of Pharmacy, Taif University, P.O. Box 11099, Taif, 21944, Saudi Arabia. h.arab@tu.edu.sa.
Sarah A Abd El-AalDepartment of Pharmacy, Kut University College, Al Kut, Wasit, 52001, Iraq.
Ahmed M AshourDepartment of Pharmacology and Toxicology, College of Pharmacy, Umm Al Qura University, P.O. Box 13578, Mecca, 21955, Saudi Arabia.
Azza A K El-SheikhBasic Health Sciences Department, College of Medicine, Princess Nourah Bint Abdulrahman University, P.O. Box 84428, Riyadh, 11671, Saudi Arabia.
Hana J Al KhabbazBiochemistry Division, College of Pharmacy, Riyadh Elm University, Riyadh, 11681, Saudi Arabia.
El-Shaimaa A ArafaCollege of Pharmacy and Health Sciences, Ajman University, 346, Ajman, United Arab Emirates.
Ayman M MahmoudPhysiology Division, Zoology Department, Faculty of Science, Beni-Suef University, Beni-Suef, Egypt.
Ahmed M KabelDepartment of Pharmacology, Faculty of Medicine, Tanta University, Tanta, 31527, Egypt.
Ajman University · AEBeni-Suef University · EGPrincess Nourah bint Abdulrahman University · SARiyadh Elm University · SATaif University · SATanta University · EGUmm al-Qura University · SAUniversity of Wasit · IQ

Funding

Taif University TURSP-2020/29
6 · The paper itself

Abstract

backgroundCardiovascular disorders are major complications of rheumatoid arthritis (RA). Hence, finding effective agents that can target RA progression and its cardiovascular consequences is demanding. The present work aimed to explore the potential of lisinopril, an angiotensin-converting enzyme inhibitor, to mitigate adjuvant's-induced arthritis with emphasis on the pro-inflammatory signals, articular degradation cues, and angiogenesis alongside JAK-2/STAT-3 and Nrf2/HO-1 pathways.

methodsLisinopril (10 mg/kg/day) was administered by oral gavage for 3 weeks and the target signals were examined by biochemical assays, ELISA, histopathology, immunoblotting, and immunohistochemistry.

resultsLisinopril attenuated the progression of arthritis as proven by lowering paw edema, arthritic index, and gait scores alongside diminishing the immune-cell infiltration/aberrant histopathology in the dorsal pouch lining. These favorable actions were associated with curtailing the production of inflammatory cytokines (TNF-α, IL-6, IL-1β, and IL-17) and the pro-inflammatory angiotensin II alongside upregulating the anti-inflammatory angiotensin-(1-7) in the hind paw of arthritic rats. At the molecular level, lisinopril inhibited the upstream JAK-2/STAT-3 pathway by downregulating the protein expression of p-JAK-2/total JAK-2 and p-STAT-3/total STAT-3 ratio and the nuclear levels of NF-κBp65. Meanwhile, lisinopril curbed the downstream cartilage degradation signals matrix metalloproteinases (MMP-3 and MMP-9) and the bone erosion cue RANKL. Equally important, the protein expression of the angiogenesis signal VEGF was downregulated in the hind paw/dorsal lining. With respect to oxidative stress, lisinopril suppressed the paw lipid peroxides and boosted GSH and Nrf-2/HO-1 pathway.

conclusionLisinopril attenuated adjuvant-induced arthritis via inhibition of inflammation, articular degradation cues, and angiogenesis.

Indexed as

Angiotensin-Converting Enzyme InhibitorsArthritis, ExperimentalArthritis, RheumatoidLisinoprilAngiotensin IIAnimalsAnti-Inflammatory AgentsCytokinesFreund's AdjuvantInflammationInterleukin-17Interleukin-6Lipid PeroxidesMatrix Metalloproteinase 3Matrix Metalloproteinase 9NF-E2-Related Factor 2Angiotensin-Converting Enzyme InhibitorsAngiotensin IIAnti-Inflammatory AgentsCytokinesFreund's AdjuvantInterleukin-17Interleukin-6Lipid PeroxidesLisinoprilMatrix Metalloproteinase 3Matrix Metalloproteinase 9NF-E2-Related Factor 2NF-kappa BTumor Necrosis Factor-alphaVascular Endothelial Growth Factor AJAK-2LisinoprilRANKLRheumatoid arthritisSTAT-3VEGF

Identifiers

PMID35764864
OpenAlexW4283694386

What Socratic holds

Textmetadata
Read underepoch 390

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 Socratic graph.