No abstract

Background: Propolis is produced by honey bees from plants, buds, and exudates and as an antiseptic is used to treat several diseases, such as acne and wounds. Objectives: Due to some difficulty in the treatment of cutaneous leishmaniasis, the aim of this study was to evaluate the propolis extract function against Leishmania major.Methods: Different concentrations (9.375, 18.75, 37.5, 75, 150, and 300 µg/mL) of both Ethanolic Extract of Propolis (EEP) and the standard drug (Glucantime) were prepared for the in vitro model, and then applied to the fixed number of promastigotes. The promastigotes were counted after 24, 48, and 72-h treatment. Then, the viability of promastigotes was tested by MTT after 72 h of treatment. Twenty mice with cutaneous leishmaniasis were divided into four groups for in vivo model, including a positive group (treatment with Glucantime), a negative group (without treatment), and two experimental groups (treatment with EEP 1% and 4%). The sizes of the ulcers were measured at the beginning of the experiment and weekly for four weeks. Results: The in vitro model indicated that both EEP and Glucantime reduced the number of promastigotes and the difference between EEP and Glucantime was not significant at concentrations 37.5, 75, 150, and 300 µg/mL. The in vivo model demonstrated that EEP 4% and Glucantime were similar and decreased the size of ulcers more significantly than the negative control and EEP 1% (P < 0.05). Conclusions: Propolis as an herbal drug had antileishmanial activity against Leishmania major in vitro and in vivo. We suggest using it for complementary treatment.

No abstract

The present study investigated the possible involvement of the nucleus accumbens' (NAc) nitric oxide system in nicotine's reversal effect upon ethanol-induced amnesia. The hypothesis was tested through ethanol state-dependent memory assessment in adult male Wistar rats. Bilateral chronic cannulae were implanted in the NAc and the animals were trained in a step-through type inhibitory avoidance memory task. The step-through latency was examined 24 h after animals' training. The pre-training or pre-test intraperitoneal (i.p.) injection of ethanol (0.9 g/kg) decreased the step-through latency, indicating an amnesic effect of the drug. Meanwhile, the pre-test administration of ethanol (0.6 and 0.9 g/kg) could reverse the pre-training ethanol (0.9 g/kg)-induced amnesia, suggesting a state-dependent effect. Similar to ethanol, the pre-test intra-NAc microinjection of nicotine (0.25 and 0.5 µg/rat) alone or nicotine (0.1, 0.25 and 0.5 µg/mouse, intra-NAc) in combination with an ineffective dose of ethanol (0.3 g/kg) could significantly reverse the (pre-training) ethanol-induced memory impairment. The ethanol (0.9 g/kg)-induced amnesia was similarly prevented following the pre-test intra-NAc administration of a nitric oxide synthase (NOS) inhibitor, L-NAME (0.4 and 0.8 µg/rat). Of note, the co-administration of L-NAME (0.04 and 0.08 µg/rat, intra-NAc) with an ineffective dose of nicotine (0.1 µg/rat, intra-NAc) could significantly potentiate the memoryimproving effect of nicotine on ethanol-induced amnesia and resembled the effects of pretest administration of a higher dose of nicotine. Furthermore, while the pre-test intra-NAc injection of L-NAME impaired the memory retrieval by itself, the pre-test intra-NAc administration of L-arginine, a nitric oxide precursor (0.3 and 0.6 µg/rat, intra-NAc), did not exert any effect either alone or in combination with an effective dose of nicotine (0.5 µg/rat, intra-NAc) on pre-training ethanol-induced memory impairment. Our findings indicated a possible role of the nucleus accumbens' nitric oxide system in the improving effects of nicotine on ethanol-induced amnesia and the related state-dependent learning.