Repository of Research and Investigative Information

Repository of Research and Investigative Information

Ilam University of Medical Sciences

Attenuation of Morphine Withdrawal Syndrome by Prosopis Farcta Extract and Its Bioactive Component Luteolin in Comparison with Clonidine in Rats

Fri Nov 8 18:48:36 2024

(2018) Attenuation of Morphine Withdrawal Syndrome by Prosopis Farcta Extract and Its Bioactive Component Luteolin in Comparison with Clonidine in Rats. Medical science monitor basic research. pp. 151-158. ISSN 2325-4416 (Electronic) 2325-4394 (Linking)

Full text not available from this repository.

Official URL: https://www.ncbi.nlm.nih.gov/pubmed/30297685

Abstract

BACKGROUND Today, the plant Prosopis farcta is frequently used for traditional medicinal purposes. The aim of this study was the identification of luteolin in P. farcta extract (PFE) and to evaluate its effect on morphine discontinuation syndrome in rats. MATERIAL AND METHODS Using high-performance liquid chromatography (HPCL), luteolin was evaluated in PFE. The frequency of behavioral symptoms of morphine withdrawal (jumping, rearing, and teeth chattering) induced by naloxone challenge were illustrated in morphine-dependent rats receiving PFE, luteolin, saline, or clonidine. LD50 of PFE and luteolin was 540 mg/kg and 150 mg/kg, respectively. Signs of behavioral morphine withdrawal in rats were significantly inhibited by chronic co-administration of PFE, luteolin, or clonidine with morphine. RESULTS This study showed that PFE was less effective than clonidine at a dose of 100 mg/kg, and at doses of 200 mg/kg and 300 mg/kg it was comparable to clonidine, and did not show a significant difference in the reduction of morphine withdrawal symptoms. Luteolin was comparable in 30 mg/kg, 60 mg/kg, and 90 mg/kg with clonidine to reduce the frequency of morphine withdrawal symptoms. PFE can be used as a source of luteolin. CONCLUSIONS The study findings suggest that PFE and luteolin might reduce the signs of narcotic withdrawal. Due to a similar effect to clonidine, its mechanism of action might be through the protein kinase A pathway and might have human therapeutic potential.

Item Type: Article
Creators:
CreatorsEmail
Moayeri, A.UNSPECIFIED
Azimi, M.UNSPECIFIED
Karimi, E.UNSPECIFIED
Aidy, A.UNSPECIFIED
Abbasi, N.UNSPECIFIED
Divisions:
Page Range: pp. 151-158
Journal or Publication Title: Medical science monitor basic research
Journal Index: Pubmed
Volume: 24
Identification Number: https://doi.org/10.12659/MSMBR.909930
ISSN: 2325-4416 (Electronic) 2325-4394 (Linking)
Depositing User: مهندس مهدی شریفی
URI: http://eprints.medilam.ac.ir/id/eprint/949

Actions (login required)

View Item View Item