Role of the intracerebroventricular injection of the visfatin and its interaction with neuropeptide Y and nitric systems on food intake in neonatal chicken.

Visfatin play an essential role in the central regulation of appetite in birds. This study aimed to determine role of intracerebroventricular (ICV) injection of the visfatin on food intake and its possible interaction with neuropeptide Y (NPY) and nitric oxide system in neonatal broiler chicken. In experiment 1, neonatal chicken received ICV injection visfatin (1, 2 and 4 µg). In experiment 2, chicken received ICV injection of B5063 (NPY1 receptor antagonist 1.25 µg), visfatin (4 µg) and co-injection of the B5063 + Visfatin. In experiments 3-6, SF22 (NPY2 receptor antagonist 1.25 µg), SML0891 (NPY5 receptor antagonist 1.25 µg), L-NAME (nitric oxide synthase inhibitor, 100 nmol) and L-arginine (Precursor of nitric oxide, 200 nmol) were injected instead of B5063. Then the amount of cumulative food was measured at 30, 60 and 120 min after injection. Obtained data showed, injection visfatin (2 and 4 µg) increased food intake compared to control group (P < 0.05). Co-injection of the B5063 + Visfatin decreased visfatin-induced hyperphagia compared to control group (P < 0.05). Co-injection of the L-NAME + Visfatin amplified visfatin-induced hyperphagia compared to control group (P < 0.05). The result showed that visfatin has hyperphagic role and this effect mediates via NPY1 and nitric oxide system in neonatal chicken.

Betaine Ameliorates Depressive-Like Behaviors in Zinc Oxide Nanoparticles Exposed Mice.

The aim of the current study was to determine protective effects of betaine on depressive-like behaviors in zinc oxide nanoparticles (ZnO NPs) exposed mice. Forty male mice randomly allocated into four experimental groups. Group 1 kept as control and groups 2-4 received oral administration of betaine (30 mg/kg), ZnO NPs (600 mg/kg), and ZnO NPs (600 mg/kg) 1 h after pre-administration of betaine (30 mg/kg) for 7 days, respectively. Then, forced swimming test (FST), tail suspension test (TST), open field test (OFT), and rotarod tests were done. Furthermore, serum malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GPx), and total antioxidant capacity (TAC) levels were determined. Hippocampal tissue samples were collected for histopathological assessment. According to the results, treatment with ZnO NPs significantly increased immobility time in the FST and TST (P<0.05). Betaine significantly decreased immobility time in the FST and TST (P<0.05). Pretreatment with betaine significantly decreased ZnO NPs-induced alterations in the FST and TST (P<0.05). The duration of staying on the rotarod and the numbers of crossings in the OFT significantly decreased in the mice that received ZnO NPs (P<0.05). These results were significantly improved in betaine+ZnO NPs treated mice as compared to the ZnO NPs group (P<0.05). Treatment with ZnO NPs significantly increased serum MDA level while decreased SOD and GPx compared to the control group (P<0.05). These changes were effectively ameliorated by pretreatment with betaine compared to the ZnO NPs group (P<0.05). No significant effect on serum TAC level was observed in all groups (P˃0.05). Administration of ZnO NPs decreased the thickness of hippocampus and pyramidal neurons in the hippocampal dentate gyrus (DG) and CA1 regions were sparsely arranged. Pretreatment with betaine caused an improvement in the histological features of the hippocampus when compared with ZnO NPs-treated mice. Taken together, these results suggest that betaine has protective role against ZnO NPs-induced toxicity in mice.

Mediatory role of the central NPY, melanocortine and corticotrophin systems on phoenixin-14 induced hyperphagia in neonatal chicken.

Animal research indicates the neuropeptide Y (NPY), corticotrophin and melanocortin systems have a mediatory role in reward, however, how these substances interact with phenytoin-14 (PNX-14) induced food intake in birds remains to be identified. Accordingly, in this research eight tests were carried out to investigate the potential interactions of the NPY, melanocortin, as well as corticotrophin systems with PNX-14 on food consumption in neonatal chickens. In the first experiment, chickens were intracerebroventricular (ICV) injected with phosphate-buffered saline (PBS) and PNX-14 (0.8, 0.16, and 3.2 nmol). In second experiment, PBS, the antagonist of CRF1/CRF2 receptors (astressin-B, 30 µg) and PNX-14 + astressin-B were injected. In the rest of the experiments chicken received astressin2-B (CRF2 receptor antagonist; 30 µg), SHU9119 (MCR3/MCR4 receptor antagonist, 0.5nomol), MCL0020 (MCR4 receptor agonist, 0.5 nmol), B5063 (NPY1 receptor antagonist, 1.25 µg), SF22 (NPY2 receptor antagonist, 1.25 µg) and SML0891 (NPY5 receptor antagonist, 1.25 µg) rather than astressin-B. Then, cumulative intake of food was recorded for 2 h. Based on the findings, PNX-14 (0.16 and 3.2 nmol) led to increment in food consumption compared with the control (P < 0.05). Co-administration of the PNX-14 and astressin-B promoted PNX-14-induced hyperphagia (P < 0.05). Co-injection of the PNX-14 + astressin2-B potentiated hyperphagia PNX-14 (P < 0.05). Co-injection of PNX-14 + B5063 inhibited the effects of the PNX-14 (P < 0.05). The co-administration of the PNX-14 and SML0891 potentiated hypophagic effects of the PNX-14 (P < 0.05). The results showed that PNX-14-induced hyperphagia mediates via NPY1, NPY5, and CRF1/CRF2 receptors in neonatal chickens.

Anti-nociceptive and antioxidant activity of betaine on formalin- and writhing tests induced pain in mice.

Pain is a physiological response which is mediated via the central and peripheral nervous system. Betaine, is a methyl glycine derivative and a commonly used nutrient supplement. The main purpose of the current paper is to determine the possible anti-nociceptive and antioxidant activity and sedative effect of betaine in mice. Adult male albino mice were divided into two categories, formalin and writhing tests. In the formalin test, mice were injected with betaine (10, 20 and 30 mg/kg) or morphine (5 mg/kg). For co-injections mice received betaine (30 mg/kg) + naloxone (2 mg/kg) or atropine (1 mg/kg), chlorpheniramine (20 mg/kg), flumazenil (5 mg/kg), cimetidine (12.5 mg/kg) and cyproheptadine (4 mg/kg). Then the formalin test was done and paw licking time was determined. In the writhing test, injections were the same but the animals were injected with acetic acid (0.6 %) and the percentage of writhing inhibition was recorded. At the end of the study, blood antioxidant levels were determined. According to the results, betaine reduced the pain response in a dose-dependent manner. Co-administration of the naloxone + betaine or flumazenil + betaine significantly decreased the anti-nociceptive effect of betaine on the licking and biting time of the injected paw and inhibited the number of writhing movements. Betaine decreased malondialdehyde (MDA) and improved superoxide dismutase (SOD) and glutathione peroxidase (GPx) levels in formalin receiving mice. No adverse locomotion and sedation effect were observed in betaine-treated mice. These findings suggest that betaine has anti-nociceptive and antioxidant activity in mice, and its anti-nociceptive role interacts with opioidergic and GABA receptors.