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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.

The present study investigated the effects of luteolin on Abeta (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 Abeta (1-40) induced memory impairment. The present results showed that luteolin (5, 10 mg/kg) has a protective effect on Abeta (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 Abeta (1-40). Taken together, the results in this study suggest that luteolin (5, 10 mg/kg) treatment improves the learning and memory in Abeta (1-40)-induced cognition deficit in rats. The ameliorating mechanisms of luteolin on Abeta (1-40)-induced amnesia may be related to activating the anti-oxidation system.

This study attempted to access the neuroprotective effect of yam (Dioscorea pseudojaponica Yamamoto) on the senescent mice induced by D-gal. The mice in the experiments were administered orally with yam (20, 100 or 500 mg/kg for 4 weeks, from the sixth week). The learning and memory abilities of the mice in Morris water maze test and the mechanisms involved in the neuroprotective effect of yam on the mice brain tissue were investigated. The content of diosgenin in the yam was also detected by using HPLC. Mice treated with yam were found to significantly improve their learning and memory abilities in Morris water maze test compared to those treated with D-gal (200 mg/kg for 10 weeks). In addition, yam was also found to increase the activities of superoxide dismutase (SOD) and glutathione peroxidase (GPx) and decrease the malondialdehyde (MDA) level on the brains of D-gal treated mice. Finally, the amount of diosgenin in the yam was 5.49 mg/g extract. To sum up, these results indicate that yam had the potential to be a useful treatment for cognitive impairment in TCM. Its beneficial effect may be partly mediated via enhancing endogenous antioxidant enzymatic activities.

The purpose of this study was to evaluate the antioxidant activity and hepatoprotective effect of ethanol extracts of Actinidia rubricaulis (AR) on chronic liver injury induced by carbon tetrachloride (CCl(4)) in rats. CCl(4) (20%, 0.5 ml/rat) was given twice a week for 8 weeks, and animals received AR throughout the entire experimental period. AR reduced the elevated levels of serum glutamate-oxalate-transaminase (sGOT) and glutamate-pyruvate-transaminase (sGPT) caused by CCl(4) at weeks 1, 3, 6, and 8. The biochemical data were consistent with those of the histological observations. The AR extract recovered the CCl(4)-induced liver injury and showed antioxidant effect in assays of antioxidant enzyme activity, such as SOD, GSH-Px and GSH-Rd. Based on these results, we suggest that the hepatoprotective effect of the AR is related to its antioxidant activity.

The aim of the present study was to search for the differential gene expression and measure the serum level of a number of biochemical parameters in the cold zheng (CZ) and non-cold zheng (NCZ) in patients receiving hemodialysis. Hemodialysis (HD) patients were randomly selected from the CZ and NCZ groups. The between-group differences in gene expression were assessed using complementary DNA (cDNA) microarray. Differential gene expression was further validated by real-time reverse transcriptase polymerase chain reaction (RT-PCR). Our results demonstrated that the up-regulation of the inflammation-associated genes, ALOX5AP, S100A8 and S100A12, down-regulation of the genes related to immunity (DEFA4), metabolism (GNG11, PYGB, PRKAR2B), and growth/proliferation (HSF2, DDR2, TK1) were found in the CZ group. Furthermore, the CZ HD patients had significantly lower serum albumin levels compared with their NCZ counterparts (3.31 +/- 0.08 g/dL versus 4.18 +/- 0.12 g/dL). It appears reasonable to conclude that up-regulated inflammatory-gene expression (ALOX5AP, S100A8 and S100A12) may play an important role in CZ HD patients.

The present study was designed to investigate the ameliorating effects of Cnidiuim monnieri L. Cusson (CM) and osthole, a constituent of CM, on the spatial performance deficit in scopolamine (SCOP)-treated or ovariectomized (OVA) rats. CM improved the deficit of spatial performance, and reversed the lower plasma estradiol levels caused by SCOP in female rats. In addition, osthole (3 and 10 mg/kg, s.c.) improved the performance deficit in OVA rats. It (10 and 30 micrograms/brain, icv) also improved the performance deficit caused by SCOP in intact female rats, and at 30 micrograms/brain improved the deficit in OVA rats. However, osthole did not alter the latency swum to reach the visible target in SCOP-treated and OVA rats. Accordingly, we suggested that osthole is an active constituent of CM, and possesses ameliorating effects on the spatial performance deficits in SCOP-treated female rats or OVA rats. The action mechanism of the effects of osthole on performance deficits was related to the estrogen-like properties and activating the central cholinergic neuronal system.

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.

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 possessed an anxiolytic effect T heanxiolytic 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 stemvia activating somatodendritic 5-HT1A autoreceptors and inhibiting postsynaptic 5-HT receptors.