Withania somnifera root extract prolongs analgesia and suppresses hyperalgesia in mice treated with morphine

Previous studies demonstrated that Withania somnifera Dunal (WS), a safe medicinal plant, prevents the development of tolerance to the analgesic effect of morphine. In the present study, we investigated whether WS extract (WSE) (100mg/kg, i.p.) may also modulate the analgesic effect induced by acute...

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Published in:Phytomedicine (Stuttgart) 2014-04, Vol.21 (5), p.745-752
Main Authors: Orrù, Alessandro, Marchese, Giorgio, Casu, Gianluca, Casu, Maria Antonietta, Kasture, Sanjay, Cottiglia, Filippo, Acquas, Elio, Mascia, Maria Paola, Anzani, Nicola, Ruiu, Stefania
Format: Article
Language:English
Subjects:
Analgesia
Analgesics, Opioid - therapeutic use
Animals
Antinociception
Binding assay
Dosage and administration
Drug Evaluation, Preclinical
Drug Synergism
Hyperalgesia
Male
Materia medica, Vegetable
Medical research
Medicine, Experimental
Mice
Morphine
Morphine - therapeutic use
Nociceptive Pain - drug therapy
Phytotherapy
Plant extracts
Plant Extracts - pharmacology
Plant Extracts - therapeutic use
Plants, Medicinal
Receptors, Neurotransmitter - agonists
Withania
Withania somnifera
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Summary:Previous studies demonstrated that Withania somnifera Dunal (WS), a safe medicinal plant, prevents the development of tolerance to the analgesic effect of morphine. In the present study, we investigated whether WS extract (WSE) (100mg/kg, i.p.) may also modulate the analgesic effect induced by acute morphine administration (2.5, 5, 10mg/kg, s.c.) in the tail-flick and in the hot plate tests, and if it may prevent the development of 2.5mg/kg morphine-induced rebound hyperalgesia in the low intensity tail-flick test. Further, to characterize the receptor(s) involved in these effects, we studied, by receptor-binding assay, the affinity of WSE for opioid (μ, δ, k), cannabinoid (CB1, CB2), glutamatergic (NMDA), GABAergic (GABAA, GABAB), serotoninergic (5HT2A) and adrenergic (α2) receptors. The results demonstrated that (i) WSE alone failed to alter basal nociceptive threshold in both tests, (ii) WSE pre-treatment significantly protracted the antinociceptive effect induced by 5 and 10mg/kg of morphine only in tail-flick test, (iii) WSE pre-treatment prevented morphine-induced hyperalgesia in the low intensity tail-flick test, and (iv) WSE exhibited a high affinity for the GABAA and moderate affinity for GABAB, NMDA and δ opioid receptors. WSE prolongs morphine-induced analgesia and suppresses the development of morphine-induced rebound hyperalgesia probably through involvement of GABAA, GABAB, NMDA and δ opioid receptors. This study suggests the therapeutic potential of WSE as a valuable adjuvant agent in opioid-sparing therapies.
ISSN:0944-7113
1618-095X
DOI:10.1016/j.phymed.2013.10.021