INHIBITORY

INHIBITORY EFFECT OF LAURUS NOBILIS ON SPONTANEOUS AND AGONIST INDUCED UTERINE CONTRACTION IN NON-PREGNANT MICE

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Abstract
Laurus nobilis (Bay leaf) is traditionally used for culinary and medicinal purposes, including the management of pain, inflammation, and menstrual disorders. Its leaves and essential oil contain bioactive compounds such as 1, 8-cineole and eugenol with known smooth muscle effects, anti-inflammatory, and antioxidant properties. Some reports suggest possible reproductive and abortifacient effects of L. nobilis. However, its direct effect on uterine contractility is not well established. Hydro-alcoholic extract was obtained from extracting the powdered leaf material with hydro-ethanol (1:1) solvent using a soxhlet apparatus. Twenty-five non-pregnant swiss albino mice were used, and those in the estrous phase (identified by vaginal smears) were sacrificed by cervical dislocation. Uterine strips were isolated, cleaned, mounted in a 10 ml organ bath containing aerated physiological saline solution maintained at 37℃, and subjected to a 40 minute equilibrium period with 0.5 g resting tension. Changes in isometric contractions were recorded using LabChart Software. The L. nobilis leaf extract (0.00625 - 0.4mg/ml) was added cumulatively to assess its effects on spontaneous, oxytocin-induced (14 nM), and high potassium-induced (80 mM) as well as oxytocin-induced
contractions in a calcium-free medium. Data were analyzed using one-way ANOVA with Dunnett’s post hoc test (p<0.05). L. nobilis leaf extract significantly and concentration-dependently reduced the amplitude and frequency of spontaneous uterine contractions and contraction induced by high KCl. It produced a slight, non-significant inhibition of oxytocin-induced contractions. In calcium-free medium, the extract markedly suppressed the frequency but only slightly reduced the amplitude of oxytocin-induced contractions. These findings indicate that L. nobilis leaf extract exerts an inhibitory effect on spontaneous and agonist-induced uterine contractions, probably through mechanisms involving blockade of extracellular calcium influx and intracellular calcium release.
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