Evidence map›Paper›PMID 41804454›Full record

ArticleDrug design, development and therapy2026

Therapeutic Potential of Cannabinoids in Attenuating Amiodarone-Induced Pulmonary Fibrosis: An in vivo Experimental Study in Wistar Rats.

Riyadh S Almalki

Abstract read
In one paragraph

Article in Drug design, development and therapy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

1 author.

Riyadh S AlmalkiDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, Umm Al-Qura University, Makkah, Saudi Arabia.ORCID 0009-0001-1803-1812

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Amiodarone (AMIO) is one of the most prescribed antiarrhythmic medications and is commonly used to treat atrial and ventricular fibrillations. A notable adverse effect of AMIO is pulmonary fibrosis. Cannabinoid (O-2545) has been shown to exert antioxidant, anti-inflammatory, and antifibrotic effects in both in vivo and in vitro experimental models. The present study aimed to investigate whether cannabinoid (O-2545) may attenuate amiodarone-induced pulmonary fibrosis in male Wistar rats. Methods: A regimen of 50 mg/kg AMIO was administered via oral gavage daily for 10 consecutive days to induce acute pulmonary fibrosis. The experiment included 24 Wistar rats assigned to four groups. The control group received daily subcutaneous injections of normal saline for the same time period. The AMIO group received a daily oral gavage of AMIO (50 mg/kg) for 10 days. Concurrently, the O-2545 group received daily oral doses of cannabinoid. The combined treatment group received both AMIO and cannabinoid orally each day for 10 days. Results: High-dose AMIO (50 mg/kg) administration resulted in a significant elevation of oxidative stress, followed by a decrease in antioxidant function, an increase in inflammatory cytokines, fibrosis markers, and apoptosis. Pro-inflammatory cytokines tumor necrosis factor alpha (TNF-α), interleukin-1β (IL-1β) and adenosine (Adens), apoptotic markers tumor protein p53 (p53) and caspase 3 protein (caspase-3), oxidative stress malondialdehyde (MDA), fibrosis indicator hydroxyproline (HYDROX), and histone deacetylase (HDAC) activity, accompanied by a marked reduction in the antioxidant glutathione (GSH), compared to the control group. Histopathological examination of pulmonary tissues revealed that O-2545 significantly mitigated AMIO-induced pulmonary fibrosis. In conclusion, the results showed that cannabinoid (O-2545) may offer significant therapeutic potential in mitigating pulmonary toxicity induced by AMIO in rats. Purpose: This study investigates the possible protective therapeutic effects of (O-2545) on AMIO-induced pulmonary fibrosis in Wistar rats.

Indexed as

AmiodaroneCannabinoidsPulmonary FibrosisAdministration, OralAnimalsAntioxidantsApoptosisDose-Response Relationship, DrugMaleOxidative StressRatsRats, WistarAmiodaroneAntioxidantsCannabinoidsadenosineamiodaronecaspase 3glutathionehistone deacetylasehydroxyprolineinterleukin-1βmalondialdehydepulmonary fibrosistumor necrosis factor alphatumor suppressor protein p53

Identifiers

PMID41804454
PMCPMC12967578

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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.