Search

This study aimed to investigate the effect of flavonoid morin on oxidative/nitrosative stress, neuroinflammation, and histological, molecular, and behavioral changes caused by amyloid-beta (Aβ) 1-42 in male Wistar rats (Alzheimer's disease model). Rats received morin (20 mg/kg, oral gavage) for 14 consecutive days after intrahippocampal injection of Aβ 1-42. Morin decreased the levels of malondialdehyde and nitric oxide, increased glutathione content, and enhanced catalase activity in the hippocampus of animals receiving Aβ 1-42. It also reduced the expression of tumor necrosis factor-α, interleukin-1β, interleukin-6, nuclear factor-kappa B, and N-methyl-D-aspartate receptor subunits 2A and 2B and increased the expression of brain-derived neurotrophic factor and α7 nicotinic acetylcholine receptor in the hippocampus of Aβ 1-42 -injected rats. Besides, morin modified neuronal loss and histological changes in the CA1 region of the hippocampus. Morin allowed Aβ 1-42 -infused rats to swim more time in the target quadrant in the Morris water maze test. It is concluded that morin may be suitable for the prevention and treatment of Alzheimer's disease by strengthening the antioxidant system, inhibiting neuroinflammation, preventing neuronal death, and enhancing memory function. [ABSTRACT FROM AUTHOR]

There are some differences between mammals and birds in terms of central food intake regulation. In avian species, the hypophagic role of nesfatin-1 has not been investigated with other neurotransmitters. Therefore, this study aimed to determine the alteration of feeding behavior following intracerebroventricular (ICV) injection of nesfatin-1 and its possible interaction with central noradrenergic, serotoninergic, and oxytocin systems in newborn broiler chicks. In experiment 1, birds received ICV injection of phosphate-buffered saline (PBS), prazosin (α 1 receptors antagonist, 10 nmol), nesfatin-1 (40 ng), and co-administration of prazosin and nesfatin-1. Experiments 2–10 were similar to experiment 1, except that yohimbine (α 2 receptors antagonist, 13 nmol), metoprolol (β 1 receptors antagonist, 24 nmol), IC1118,551 (β 2 receptors antagonist for, 5nmol), SR59230R (β 3 receptors antagonist, 20 nmol), fluoxetine (serotonin reuptake inhibitor, 10 µg), PCPA (serotonin synthesis inhibitor, 1.5 µg), 8-OH-DPAT (5-HT 1 A receptors agonist, 15.25 nmol), SB242084 (5-HT 2 C receptors antagonist,1.5 µg) and tocinoic acid (oxytocin receptors antagonist, 2 µg) were injected instead of prazosin. Immediately after the injection, food consumption and behavioral traits were recorded. Nesfatin-1 decreased food consumption (P < 0.05). Nesfatin-1 along with ICI118551 decreased food consumption (P < 0.05). The nesfatin-1- induced hypophagia were reduced by the simultaneous injection of PCPA and nesfatin-1 (P < 0.05). Nesfatin-1induced hypophagia were decreased by the simultaneous injection of SB242084 (P < 0.05). The nesfatin-1 -induced hypophagia were abolished by the simultaneous injection of the tocinoic acid and nesfatin-1 (P < 0.05). ICV injection of the nesfatin-1 decreased the number of steps, jumps, exploratory food, and pecks (P < 0.05) with no effect on drink pecks (P > 0.05). Nesfatin-1 significantly decreased standing time and increased both sitting time and rest time (P < 0.05). Nesfatin-1 could play an important role in feeding behavior, and its hypophagic effects were mediated by β 2 adrenergic, 5-HT 2 C serotoninergic, and oxytocin receptors in neonatal chickens. • Central injection of Nesfatin-1 reduced food intake with no effect on drink pecks. • Co-administration of the β 2 receptor antagonist and nesfatin-1 reduced hypophagic effects of nesfatin-1. • Co-administration of 5-HT 2 C receptor agonist and nesfatin-1 inhibited the hypophagic effects of nesfatin-1. • Co-administration of OXT receptor antagonist and nesfatin-1 inhibited hypophagic effect of the nesfatin-1. • Nesfatin-1 decreased number of steps, jumps, exploratory food and pecks. [ABSTRACT FROM AUTHOR]