Effects of ghrelin on sexual behavior and luteinizing hormone beta-subunit gene expression in male rats

Background: The hormones of hypothalamo-pituitary-gonadal [HPG] axis have facilitative effects on reproductive behavior in mammals. Ghrelin as a starvation hormone has an inhibitory effect on HPG axis' function. Hence, it is postulated that ghrelin may reduce the sexual behavior through inhibiting of HPG axis. The aim of this study was to examine the effects of ghrelin and its antagonist, [D-Lys3]-GHRP-6, on sexual behavior and LH beta-subunit gene expression in male rats

Methods: In this experimental study, 128 male Wistar rats were divided into two groups. Each group was further subdivided into eight subgroups [n=8 rats/subgroup] including the animals that received saline, ghrelin [2, 4 or 8 nmol], [D-Lys3]-GHRP-6 [5 or 10 nmol] or co-administration of ghrelin [4 nmol] and [D-Lys3]-GHRP-6 [5 or 10 nmol] through the stereotaxically implanted cannula into the third cerebral ventricle. The sexual behavior of male rats encountering with females and the hypophyseal LH beta-subunit gene expression were evaluated at two different groups

Data were analyzed by ANOVA and p<0.05 was considered statistically significant. Results: Ghrelin injection [4 and 8 nmol] significantly [p<0.01] increased the latencies to the first mount, intromission and ejaculation as well as the post-ejaculatory interval. Also, 4 and 8 nmol ghrelin significantly [p<0.05] increased the number of mount and decreased the number of ejaculation. In co-administrated groups, [DLys3]- GHRP-6 antagonized the effects of ghrelin. Ghrelin injection [4 and 8 nmol] reduced the LH beta-subunit gene expression while pretreatment with [D-Lys3]- GHRP-6 improved the gene expression

Conclusion: Ghrelin decreased the sexual behavior and LH beta-subunit gene expression in male rats, whereas [D-Lys3]-GHRP-6 antagonizes these effects

Effects of melatonin and vitamin E on peripheral neuropathic pain in streptozotocin-induced diabetic rats

Previous studies have indicated that diabetes mellitus might be accompanied by neuropathic pain. Oxidative stress is implicated as a final common pathway in development of diabetic neuropathy. Pharmacological interventions targeted at inhibiting free radical production have shown beneficial effects in diabetic neuropathy. The aim of this study was to investigate and compare the possible analgesic effects of melatonin and vitamin E in diabetic rats. This study was performed on 32 male Wistar rats divided into 4 groups: control, diabetic, melatonin-treated diabetic and vitamin E-treated diabetic. Experimental diabetes was induced by intraperitoneal streptozotocin [50 mg/kg] injection. Melatonin [10 mg/kg, i.p.] and vitamin E [100 mg/kg, i.p.] were injected for 2 weeks after 21 st day of diabetes induction. At the end of administration period, pain-related behavior was assessed using 0.5% formalin test according to two spontaneous flinching and licking responses. The levels of lipid peroxidation as well as glutathione-peroxidase and catalase activities were evaluated in lumbosacral dorsal root ganglia. Formalin-evoked flinching and total time of licking were increased in both acute and chronic phases of pain in diabetic rats as compared to control rats, whereas treatment with melatonin or vitamin E significantly reduced the pain indices. Furthermore, lipid peroxidation levels increased and glutathione-peroxidase and catalase activities decreased in diabetic rats. Both antioxidants reversed the biochemical parameters toward their control values. These results suggest that oxidative stress may contribute to induction of pain in diabetes and further suggest that antioxidants, melatonin and vitamin E, can reduce peripheral neuropathic pain in streptozotocin-induced diabetic rats