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2007年05月21日

【期刊论文】Ethanol and acetaldehyde induce similar changes in extracellular levels of glutamate, taurine and GABA in rat anterior cingulate cortex

吴春福, Gong Cheng Zuo, Jing Yu Yang, Yue Hao, Ying Xu Dong, Chun Fu Wu

G. C. Zuo et al. Toxicology Letters 169 (2007) 253-258,-0001,():

-1年11月30日

摘要

It is controversial regarding to the roles of acetaldehyde and ethanol in the central nervous system. In the present study, the effects of acetaldehyde and ethanol on extracellular levels of glutamate, taurine and GABA in the anterior cingulate cortex (ACC) of freely moving rats were investigated by using the microdialysis technique coupled to high performance liquid chromatography (HPLC) with fluorescent detection. The result showed that glutamate levels were significantly decreased after acute administration of acetaldehyde (AcH, 20 and 100mg/kg, i.p.), while taurine levels were significantly increased after the higher dose of acetaldehyde (100mg/kg, i.p.). GABA levels had no changes at any doses of acetaldehyde tested. Interestingly, similar changes of these amino acids were induced by ethanol (EtOH, 3g/kg, i.p.) when sodium azide (NaN3, 10mg/kg, i.p.), a catalase inhibitor that can reduce brain ethanol metabolism, was used simultaneously. These findings suggest that acetaldehyde and ethanol have the similar effects on the extracellular output of glutamate, taurine and GABA in the ACC.

Acetaldehyde, Ethanol, Glutamate, Taurine, GABA, Anterior cingulate cortex

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2007年05月21日

【期刊论文】Endogenous released ascorbic acid suppresses ethanol-induced hydroxyl radical production in rat striatum

吴春福, Mei Huang, Wen Liu, Qiang Li, Chun Fu Wu

M. Huang et al. Brain Research 944 (2002) 90-96,-0001,():

-1年11月30日

摘要

Previous studies have shown that acute systemic administration of ethanol induced ascorbic acid release in the striatum. However, the pharmacological implications of ethanol-induced striatal ascorbic acid release are unclear. In the present study, ethanol-induced extracellular changes of ascorbic acid and hydroxyl radical levels were detected in rat striatum by using brain microdialysis coupled to high-performance liquid chromatography with electrochemical detection. It was found that both in male and female rats, ethanol (3.0g/kg, i.p.) increased striatal ascorbic acid release in the first 60 min after ethanol administration. Meanwhile, the extracellular hydroxyl radical levels, detected as 2, 3- and 2, 5-DHBA, were significantly decreased. However, when the ascorbic acid levels returned to the baseline, hydroxyl radical levels rebounded. Administration of DL-fenfluramine (20mg/kg, i.p.) had no effect on the basal levels of ascorbic acid and hydroxyl radical, but significantly blocked ethanol-induced ascorbic acid release and increased hydroxyl radical levels significantly. Exogenous administration of ascorbic acid (20mg/kg, s.c.) increased the extracellular levels of ascorbic acid in the striatum, and inhibited the increase of 2, 3- and 2, 5-DHBA in DL-fenfluramine plus ethanol group. These results provide first evidence that release of endogenous ascorbic acid in the striatum plays an important role in preventing oxidative stress by trapping hydroxyl radical in the central nervous system.

Ethanol, Ascorbic acid, Hydroxyl radical, DL-Fenfluramine, Striatum, Microdialysis (, rat),

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2007年05月21日

【期刊论文】Effects of Fructus Ligustri Lucidi Extract on Bone Turnover and Calcium Balance in Ovariectomized Rats

吴春福, Yan ZHANG, , Wan-Ping LAI, Ping-Chung LEUNG, Chun-Fu WU, Xin-Sheng YAO, and Man-Sau WONG

Biol. Pharm. Bull. 29 (2) 291-296 (February 2006),-0001,():

-1年11月30日

摘要

The aim of this study was to evaluate the effect of Fructus Ligustri Lucidi (FLL), a kidney-tonifying Chinese herbal medicine, on the biochemical markers of bone turnover, calcium metabolism and balance in osteoporotic rat model developed by ovariectomy. Four weeks after surgical operation, animals were randomly assigned to one of the four treatments for 14 weeks: sham-operated control treated with vehicle (sham, n=8), ovariectomized group treated with vehicle (OVX, n=8), OVX group treated with 17β-estradiol (E2, n=10, 2μg/kg/d) and OVX group treated with FLL extracts (FLL, n=10, 550mg/kg/d). Serum osteocalcin and urinary deoxypyridinoline levels were upregulated in rats in response to OVX, suggesting that the bone turnover rate was accelerated in these animals. Treatment of OVX rats with FLL extract could prevent OVX-induced increase in bone turnover by suppression of both serum osteocalcin (p<0.05, vs. OVX) and urinary deoxypyridinoline (p<0.05, vs. OVX) levels. In addition, FLL extract could prevent OVX-induced loss of calcium in rats by increasing the intestinal calcium absorption rate (p<0.01, vs. OVX), suppressing urinary Ca excretion (p<0.05, vs. OVX) as well as increasing bone calcium content (p<0.05, vs. OVX). Our study is the first to report that FLL can modulate bone turnover and calcium balance in OVX rats and it might be a potential candidate for prevention and treatment of postmenopausal osteoporosis.

Fructus Ligustri Lucidi, ovariectomy, bone turnover, calcium balance

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2007年05月21日

【期刊论文】Effects of clozapine, olanzapine and haloperidol on nitric oxide production by lipopolysaccharide-activated N9 cells

吴春福, ue Hou, , Chun Fu Wu, Jing Yu Yang, Xiang He, Xiu Li Bi, Liang Yu, Tao Guo

Y. Hou et al. Progress in Neuro-Psychopharmacology & Biological Psychiatry xx (2006) xxx-xxx,-0001,():

-1年11月30日

摘要

Schizophrenia is a devastating illness of unknown etiology and the basis for its treatment rests in the symptomatic response to antipsychotics. It was found that some of the patients with schizophrenia elicited microglia activation. The present study used lipopolysaccharide (LPS)-activated mouse microglial cell line N9 as an in vitro model to mimic microglia activation seen in the patients with schizophrenia. The effects of clozapine, olanzapine and haloperidol on the release of nitric oxide (NO) by LPS-stimulated N9 cells were investigated. The results showed that olanzapine significantly inhibited NO release by LPS-stimulated N9 cells. Clozapine and haloperidol did not show significant effects on this model. The present study suggested that the inhibiting effect of olanzapine on the NO release by LPS-stimulated microglial cells might be a new mechanism through which olanzapine exhibits its therapeutic effect in the treatment of schizophrenia.

Clozapine, Haloperidol, N9 cells, Nitric oxide (, NO), , Olanzapine

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2007年05月21日

【期刊论文】Effect of drug-induced ascorbic acid release in the striatum and the nucleus accumbens in hippocampus-lesioned rats

吴春福, Fang Dai, Jing Yu Yang, Pei Fei Gu, Yue Hou, Chun Fu Wu

BRAINRESEARCH 1125 (2006) 163-170,-0001,():

-1年11月30日

摘要

The mechanism of ethanol, morphine, methamphetamine (MAP), and nicotine-induced ascorbic acid (AA) release in striatum, and nucleus accumbens (NAc) is not well understood. Our previous study showed that the glutamatergic system was involved in the addictive drug-induced AA release in NAc and striatum. Furthermore, frontal decortication eliminates drug-induced ascorbic acid release in the striatum but not in the NAc. In the present study, the roles of the hippocampus in drug-induced AA release in the striatum and NAc were studied by using microdialysis coupled to high performance liquid chromatography with electrochemical detection (HPLC-ECD). Ethanol (3.0 g/kg, i.p.), methamphetamine (3.0 mg/kg, i.p.), and nicotine (1.5 mg/kg, i.p.) significantly stimulated AA release in the striatum and NAc, respectively. Morphine (20 mg/kg, i.p.) significantly stimulated AA release in the striatum, but not in the NAc. After hippocampal lesion by kainic acid, AA release induced by ethanol, methamphetamine, and nicotine could be eliminated in NAc, but not in the striatum. These results suggest that the hippocampus might be a common and necessary area in addictive drug-induced AA release in the NAc, which also imply that different pathways might be involved in drug-induced AA release in the striatum and the NAc of the rats.

Ascorbic acid,, Striatum,, Nucleus accumben,, Ethanol,, Morphine,, Methamphetamine

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  • 吴春福 邀请

    沈阳药科大学,辽宁

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