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This study attempted to access the neuroprotective effect of diosgenin on the senescent mice induced by d-galactose (D-gal). The mice in the experiments were orally administered with diosgenin (1, 5, 25 and 125 mg/kg), for four weeks from the sixth week. The learning and memory abilities of the mice in Morris water maze test and the mechanism involved in the neuroprotective effect of diosgenin on the mice brain tissue were investigated. Diosgenin (5, 25 and 125 mg/kg, p.o.) showed significantly improved learning and memory abilities in Morris water maze test compared to D-gal treated mice (200 mg/kg, ten weeks). Diosgenin also increased the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), and decreased the malondialdehyde (MDA) level in the brain of D-gal treated mice. These results indicated that diosgenin has the potential to be a useful treatment for cognitive impairment. In addition, the memory enhancing effect of diosgenin may be partly mediated via enhancing endogenous antioxidant enzymatic activities. [ABSTRACT FROM AUTHOR]

The present study investigated the effects of luteolin on Aβ (1-40)-induced impairment of Morris water maze (MWM) spatial performance, reference memory, and passive avoidance (PA) behavior in rats. Luteolin treatment was started 4 days before the initiation of behavioral testing (passive avoidance on treatment day of 4–5; MWM spatial performance memory testing on treatment day of 5–7 and MWM reference memory testing on treatment day of 7) and continued until the end of the study. We also measured the activity of Mn-SOD, copper/zinc (Cu/Zn)-SOD and glutathione (GSH) levels in rat cortex and hippocampus to understand the ameliorating effect of luteolin on Aβ (1-40) induced memory impairment. The present results showed that luteolin (5, 10 mg/kg) has a protective effect on Aβ (1-40)-induced memory dysfunction in spatial performance, reference memory, and inhibitory avoidance response impairment. Finally, luteolin also increases the level of Mn-SOD, (Cu/Zn)-SOD and glutathione (GSH) in the cortex and hippocampus to reduce the oxidative stress by Aβ (1-40). Taken together, the results in this study suggest that luteolin (5, 10 mg/kg) treatment improves the learning and memory in Aβ (1-40)-induced cognition deficit in rats. The ameliorating mechanisms of luteolin on Aβ (1-40)-induced amnesia may be related to activating the anti-oxidation system. [ABSTRACT FROM AUTHOR]

The study was to investigate the ameliorating effects of three Chinese herbs — Achyranthes bidentata (AB), Ophiopogon japonicus (OJ) and Cnidium monnieri (CM) on scopolamine (SCOP)- and MK-801-induced amnesia by using a passive avoidance task in rats. AB, OJ and CM at 0.1 and 0.3 g/kg prolonged the step-through latency (STL) of the retention trial. In addition, AB, OJ and CM reversed the STL shortened by MK-801, but only AB reversed the STL shortened by SCOP. In conclusion, these Chinese herbs possess cognition-enhancing activities and anti-amnestic effects, but the mechanism of the effect of AB was different from those of OJ and CM. [ABSTRACT FROM AUTHOR]

The anxiolytic effect of the alcoholic extract of Ting-Chih-Wan (TCWa) was studied using the black and white test (BWT) and the elevated plus-maze (EPM). We further demonstrated the anxiolytic mechanism of TCWa by combining with diazepam (DIZ), serotonin (5-HT) agonists or antagonists, and measuring the levels of monoamines and its metabolites in the brain stem and cortex. In the BWT, TCWa (0.1–1.0 g/kg, p.o.) increased the time spent in the white chamber and total change between the two chambers, and decreased the time spent in the black chamber. TCWa (0.1–0.5 g/kg, p.o.) increased the arm entries and the time spent on the open arms, and decreased the arm entries and the time spent on the closed arms in the EPM. On the other hand, TCWa (1.0 g/kg, p.o.) decreased horizontal activity and prolonged pentobarbital-induced sleeping times. TCWa (0.1, 0.5 g/kg) decreased the levels of norepinephrine (NE), dopamine (DA), 5-HT and 5-hydroxy-indoleacetic acid (5-HIAA) and increased the levels of vanillylmandelic acid (VMA) and homovanillic acid (HVA) in the brain stem. TCWa (0.1 and 0.5 g/kg) decreased the levels of NE, DA and increased the levels of VMA and HVA in the cortex. TCWa also attenuated the anxiogenic effect of 5-hydroxytryptophan (5-HTP) and enhanced the anxiolytic effect of 9p-chlorophenylalanine (PCPA), buspirone (BUS) and ritanserin (RIT) in the EPM. From these results, TCWa at 0.1 and 0.5 g/kg posessed an anxiolytic effect. The anxiolytic mechanisms of TCWa might be due to decreased catecholaminergic activity caused by the increase in the turnover rate of catecholamines in the brain and decreased concentrations of 5-HT in the brain stem via activating somatodendritic 5-HT1A autoreceptors and inhibiting postsynaptic 5-HT2 receptors. [ABSTRACT FROM AUTHOR]