OBJECTIVE:The effects of zinc fructose diphosphate(ZnFDP)in different concentrations on the growth of cultured newborn mouse cerebral cortex neurons were observed METHODS:The newborn mice cerebral cortex neurons were cultured and different dosages of ZnFDP were added with final concentrations of 2 5?g/ml,12 5?g/ml and 125?g/ml The convert phase microscope was used to observe the growth of dendrites and cell bodies of neurons The survival neuron count and LDH assay were carried out to investigate the effect of ZnFDP on the growth and development of neurons in different culture periods RESULTS:After 48h,the number and the length of neural dendrites in 12 5?g/ml ZnFDP group were increased but the maximum diameter of cell bodies of neurons showed no change There were no significant differences in all parameters observed between 2 5?g/ml group and control group,while 125?g/ml ZnFDP obviously inhibited the differentiation of neurons The survival neurons on 12 5?g/ml ZnFDP group outnumbered those in the control group after 3d,7d and 10d culture,and the LDH activity in 12 5?g/ml ZnFDP group was lower than that in control group after 7d and 10d culture CONCLUSION:This study suggests that a suitable dose of ZnFDP can promote the growth and development of cerebral cortex neurons

Alzheimer's disease (AD) is a kind of neurodegenerative diseases, the most common cause of dementia. Although AD has been studied more than, 100 years and the Aβ and tau theory are most widely accepted among the theories achieved, yet it is not really clear what the mechanism related to AD works up to now. However, it is certain that AD is a kind of diseases resulting from multi-causes. Except for causes correlated with heredity, aging and life habits, environmental role is worth taking into consideration as well. Some metals, such as copper, aluminum, zinc and iron et al, can also have close relationship with AD. Now, we make an overview on the correlative researches in the field.

Alzheimer's disease is a neurodengenerative disorder disease with the progressive cognition malfunction and memory impairmen t. This article analyze the biochemical cause of Alzheimer's disease and eval uate the current status of drug therapy for the disease, and predict the possi bili ty of RNA interference in the therapy of Alzheimer's disease.

AIM: This study was designed to investigate the inhibition of tanshinone ⅡA on C6 glioma cell line and its mechanism. METHODS: MTT was used to measure the levels of the proliferation of C6 cultured with tanshinone ⅡA at different concentrations. The effects of tanshinone ⅡA on cell cycle of C6 were observed by FCM. The change of DNA was observed by Sepharose electrophoresis. The expression of proto-oncogenes c-myc was measured by RT-PCR. RESULTS: The proliferation of C6 was obviously inhibited by tanshinone ⅡA in a dose-dependent manner. The outcome of FCM showed that the apoptotic cell rate was 7.7%, when cultured with tanshinone ⅡA at 1.0 mg/L for 3 days. The apoptotic cell rate was 21.6%, when cultured with tanshinone ⅡA at 2.0 mg/L in 3 days. CONCLUSION: Tanshinone ⅡA inhibits the proliferation of C6 cells, induces apoptosis and inhibits the expression of proto-oncogene c-myc.

AIM: To discover specific neural stem cell (NSC) proliferation-promoting factor, which will contribute to study on development of nervous system and treatment of nervous system diseases. METHODS: The extracts of forebrain, midbrain,afterbrain and cerebellum of neonatal mice were prepared, and the NSCs of newborn mice were cultured in vitro. Neurospheres were observed, immunocytochemical staining of characteristic protein, nestin, and MTT assay were performed to identify NSCs and their proliferative properties. RESULTS: A great deal of neurospheres were formed in the presence of the extracts of afterbrain and cerebellum, which were positive for characteristic protein (Nestin) of NSC showed by immunocytochemical staining. CONCLUSION: The afterbrain and cerebellum extracts can increase the total number of NSCs isolated from newborn mice in vitro in a dose-dependent manner.

Aim This study was designed to investigate the inhibition of matrine on U251 glioma cell line and its mechanism. Methods MTT was used to measure the levels of the proliferation of U251 cultured with matrine in different concentrations.The effects of matrine on cell cycle of U251 were observed by FCM. The expression of proto oncogenes c myc was measured by RT PCR. Results The proliferation of U251 was obviously inhibited by matrine in a dose dependent manner. The inhibitory rate was (53 7?6 0)%,when cultured with matrine at 0 10 g?L -1 . The outcome of FCM showed that the proportion of G 0/G 1 phase cells were decreased. The proportion of S phase cells were reduced obviously,when cultured with matrine at 0 10 g?L -1 in 3 days.The outcome of RT PCR showed that the expression of proto onco gene C myc was notably decreased, when the dose of matrine was increased. Conclusion Matrine can inhibit the proliferation of U251 and inhibit the expression of proto onco gene C myc.

Aim The pharmacodynamics and mechanism of Kadsura heteroclita on the Alzheimers disease (AD) model mice were studied. Methods The Kunming mice were treated with D-galactose and AlCl 3(90 d)to make the AD animal model. The therapy groups were treated with HS 2 (po, 40 d) respectively since d51. The Morris water-maze test, the expressions of PS1, BACE, as well as the pathological observation of the hippocampus and cerebral cortex were carried out to evaluate the effect of HS 2 on the AD model mice. Resluts By oral administration with HS 2, the capacity of learning and memory of the AD model mice was improved. HS 2 can downregulate the expression of PS1, BACE and decrease the amount of senile plaque in their brains. Conclusion HS 2 can meliorate AD model mice's learning and memory deficiency as well as decrease the mRNA content of PS1, BACE and senile plaque in their brains.

AIM: This study was designed to investigate the effect of ginsenoside Rg1 on the amyloid ?-protein precursor (APP) and neprilysin (NEP)expression induced by lipopolysaccharide (LPS) in C6 cell line in order to discover effectual Alzheimer's disease (AD)-treated drugs. METHODS: MTT colorimetric analysis was used to measure the survival rate of C6 cultured with ginsenoside Rg1 at different concentrations (2 5, 5, 10 and 20 ?mol?L -1) and LPS (100 mg?L -1). The expression of APP and NEP mRNA was measured by RT-PCR. RESULTS: LPS decreased the survival rate of C6, furthermore, the increase in APP expression and the decrease in NEP expression were observed. On the other hand, the above alteration induced by LPS was reversed by ginsenoside Rg1. CONCLUSION: This study demonstrates that LPS can cause cell damage, the increase in APP expression and the decrease in NEP expression. Ginsenoside Rg1 can exert a neuroprotective action, protect C6 cells against LPS-induced injury via inhibiting APP expression and increasing NEP expression.

AIM: To investigate the inhibitory effect of TanshinoneⅡA on U251 glioma cell line and its mechanism. METHODS: MTT was used to measure the levels of the proliferation in U251 cultured with TanshinoneⅡA at different concentrations. The effects of TanshinoneⅡA on cell cycle of U251 were observed by FCM. The expression of proto-oncogene c-myc was measured by RT-PCR. RESULTS: The proliferation of U251 was obviously inhibited by TanshinoneⅡA in a dose dependent manner. The inhibitory rate came to the peak at (54 2?0 9)%, when cultured with TanshinoneⅡA at 0 10 g/L. The outcome of FCM showed that the proportion of G 0/G 1 phase cells was increased and the proportion of S phase cells was reduced obviously, when cultured with TanshinoneⅡA at 0 10 g/L for 3 days. The RT-PCR experiment showed that the expression of proto-oncogene c-myc was notably decreased, when the dose of TanshinoneⅡA was increased. CONCLUSION: TanshinoneⅡA inhibited the proliferation of U251 and the expression of proto-oncogene c-myc.

OBJECTIVETo study the liposoluble ingredients of Quchiling (LQ), which enter the blood and the brain,and to confirm the active ingredients of LQ in vivo.

METHODSerum pharmacochemistry and gas chromatography mass spectroscopy were used to analyze ingredients of LQ entering the blood and the brain.

RESULTThere were eleven ingredients of LQ to enter the blood and six ingredients of LQ to enter the brain.

CONCLUSIONIt is confirmed that eleven ingredients of LQ entered the blood, which are beta-asarone, schisandrol A, schisandrol B, deoxyschisandrin, schisandrin B, schisantherrin A, schisantherrin B, schisantherrin C, delta-cadinene, delta-cadinol and calamendiol in the blood, and that six ingredients are beta-asarone, schisandrol A, schisandrol B, deoxyschisandrin, schisandrin B and calamendiol in the brain.

Animals ; Anisoles ; chemistry ; metabolism ; Brain ; metabolism ; Cyclooctanes ; chemistry ; metabolism ; Dioxoles ; chemistry ; metabolism ; Drugs, Chinese Herbal ; chemistry ; metabolism ; pharmacokinetics ; Female ; Gas Chromatography-Mass Spectrometry ; Lignans ; chemistry ; metabolism ; Male ; Polycyclic Compounds ; chemistry ; metabolism ; Rats ; Rats, Sprague-Dawley