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The present study investigated the impact of carnosic acid (CA) from rosemary on the levodopa (L-dopa)-induced dyskinesia (LID) in rats treated with 6-hydroxydopamine (6-OHDA). To establish the model of LID, 6-OHDA-lesioned rats were injected intraperitoneally with 30 mg/kg L-dopa once a day for 36 days. Rats were daily administrated with 3 or 15 mg/kg CA by oral intubation prior to L-dopa injection for 4 days. Rats pretreated with CA had reduced L-dopa-induced abnormal involuntary movements (AIMs) and ALO scores (a sum of axial, limb, and orofacial scores). Moreover, the increases of dopamine D1-receptor, p-DARPP-32, ΔFosB, p-ERK1/2, and p-c-Jun ser63, along with the decrease in p-c-Jun ser73, induced by L-dopa in 6-OHDA-treated rats were significantly reversed by pretreatment with CA. In addition, we used the model of SH-SY5Y cells to further examine the neuroprotective mechanisms of CA on L-dopa-induced cytotoxicity. SH-SY5Y cells were treated with CA for 18 h, and then co-treated with 400 μM L-dopa for the indicated time points. The results showed that pretreatment of CA attenuated the cell death and nuclear condensation induced by L-dopa. By the immunoblots, the reduction of Bcl-2, p-c-Jun ser73, and parkin and the induction of cleaved caspase 3, cleaved Poly (ADP-ribose) polymerase, p-ERK1/2, p-c-Jun ser63, and ubiquitinated protein by L-dopa were improved in cells pretreated with CA. In conclusion, CA ameliorates the development of LID via regulating the D1R signaling and prevents L-dopa-induced apoptotic cell death through modulating the ERK1/2-c-Jun and inducing the parkin. This study suggested that CA can be used to alleviate the adverse effects of LID for PD patients. [ABSTRACT FROM AUTHOR]

The present study investigated the ameliorating effects of p-hydroxybenzyl alcohol (HBA), an active phenolic ingredient of Gastrodia elata, on cycloheximide (CXM)-induced impairment of passive avoidance response and clarified the role of adrenal glands on the effect of HBA in rats. An adrenalectomy (ADX) caused the memory deficit from 1 to 3 days after surgery. Administration of corticosterone (CORT) plus glucose completely recovered the memory deficit caused by ADX, and this effect was better than that of glucose or CORT alone. HBA ameliorated the memory deficit induced by CXM in sham and ADX rats, but ADX partially blocked it. Furthermore, plasma glucose, epinephrine and adrenal steroid levels of ADX rats significantly decreased. Sham rats who received HBA had an increase in plasma glucose and adrenal steroid levels. Therefore, we suggest that the reversal of CXM-induced memory deficit by HBA was partially dependent on adrenal glands through the increase of the levels of plasma adrenal steroids. [ABSTRACT FROM AUTHOR]

Cholinergic dysfunction and oxidation stress are the dominant mechanisms of memory deficit in Alzheimer's disease (AD). This study describes how ferulic acid (FA) ameliorates cognitive deficits induced by mecamylamine (MECA), scopolamine (SCOP), central acetylcholinergic neurotoxin ethylcholine mustard aziridinium ion (AF64A) and amyloid β peptide (Aβ1-40). This study also elucidates the role of anti-oxidant enzymes and cholinergic marker acetylcholinesterase (AChE) in the reversal of FA from Aβ1-40-induced cognitive deficits in rats. At 100 mg/kg, FA attenuated impairment induced by MECA and SCOP plus MECA; however, this improvement was not blocked by the peripheral muscarinic receptor antagonist scopolamine methylbromide (M-SCOP). At 100 and 300 mg/kg, FA also attenuated the impairment of inhibitory passive avoidance induced by AF64A. Further, FA attenuated the performance impairment and memory deficit induced by Aβ1-40 in rats, as did vitamin E/C. FA reversed the deterioration of superoxide dismutase (SOD) and AChE activities, and the glutathione disulfide (GSSG) and glutathione (GSH) levels in the cortex and hippocampus. Vitamin E/C only selectively reversed deterioration in the hippocampus. We suggest that FA reduced the progression of cognitive deficits by activating central muscarinic and nicotinic receptors and anti-oxidant enzymes. [ABSTRACT FROM AUTHOR]

Ligustrum morrisonense Kaneh and Sasaki (abbreviated as LM), an endemic Ligustrum plant in Taiwan, is similar to Ligustrum lucidum, which is usually used for curing hepatic and inflammatory disorders. The aim of this study was to evaluate the analgesic and anti-inflammatory properties of LM by chemical-induced algesia and carrageenan-induced inflammation in rodents. Its triterpenoid contents were measured by using high performance liquid chromatography-photodiode array detector. LM leaf extracts effectively inhibited writhing responses induced by 1% acetic acid and biphasic-licking responses caused by 1% formalin. LM leaf extract also reduced the edema induced by 1% carrageenan. Furthermore, LM leaf extract reduced the abdominal Evan's blue extravasations caused by lipopolysaccharide (LPS), serotonin, histamine and bradykinin. LM leaf extract has higher contents of amyrin and lupeol among six assayed triterpenoid compounds. In conclusion, LM is a potential analgesic and anti-inflammatory Ligustrum plant, and its anti-inflammatory effects are partially related to decreasing microvascular permeability via inflammatory mediators and inhibiting cyclooxygenase-2 activity. [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 concentrations of monoamines in the striatum, dorsal raphe and cortex of the brain of male Sprague-Dawley rats were monitored using in vivo microdialysis before, during and after noise exposure. Some 120 h after implantation of the microdialysis probe in the desired area, the rats were exposed to white noise (110 dB) for 20 min. The concentrations of monoamines in the dialysate were determined by HPLC. Exposure to white noise increased epinephrine in the striatum (42%) and dorsal raphe (39%), values then declined to baseline. In contrast, white noise decreased 3,4-dihydroxyphenylacetic acid (DOPAC) in the striatum (99%) and cortex (53%); these levels remained depressed following noise cessation. Noise also decreased homovanillic acid (HVA) in the striatum and in 5-hydroxy-indoleacetic acid (5-HIAA) in the striatum and dorsal raphe nucleus. Other neurotransmitters (norepinephrine etc.) did not change significantly in any region. These results suggest that noise influences monoamine levels differently in different brain regions. [ABSTRACT FROM AUTHOR]

Abstract: The study was conducted to investigate the ameliorating effects of luteolin on memory acquisition in rats. The effects of luteolin on scopolamine-induced impairment of passive avoidance response were evaluated primarily, as well as the role of the central nervous system through the use of central neurotoxins and central nervous antagonists. Luteolin was not reversed by scopolamine N-methylbromide (M-SCOP) but blocked the impairment of learning acquisition induced by cholinergic neurotoxin (ethylcholine aziridinium, AF64A) and muscarinic (scopolamine hydrobromide, SCOP) and nicotinic (mecamylamine, MECA) receptor antagonists. However, it did not block dopaminergic neurotoxin (6-hydroxydopamine, 6-OHDA)-induced and serotonergic neurotoxin (5,7-dihydroxytryptamine, 5,7-DHT)-induced impairments. From these results, we suggest that the attenuating effect of luteolin (10 mg/kg, i.p.) on the deficits of passive avoidance performance induced by SCOP may be related to the increases in the activities of central muscarinic and nicotinic receptors. [Copyright &y& Elsevier]