共查询到20条相似文献，搜索用时 218 毫秒
1.
AIM:To investigate the inhibitory effect of 4-phenylbutyric acid (4-PBA), an aromatic short-chain fatty acid with the functions of endoplasmic reticulum (ER) molecule chaperon, on ER stress-induced decreases in both dendritic spine density and synaptic protein expression. METHODS:Primary hippocampal neurons were cultured from neonatal rats. The primary hippocampal neurons were transfected with enhanced green fluorescent protein plasmids at DIV (day in vitro) 5~7. At DIV 20, the neurons were divided into DMSO group, tunicamycin group and tunicamycin+4-PBA (treated with 4-PBA 1 h before tunicamycin) group. The expression levels of ER stress marker protein BiP and synaptic proteins were detected by Western blot. After immunofluorescence staining, the neurons were morphologically observed under confocal laser scanning microscope, and the density of dendritic spines was analyzed. At last, the cell viability was measured by MTT assay. RESULTS:Tunicamycin induced ER stress in the primary hippocampal neurons, characterized by significantly increased level of BiP in tunicamycin group, which was reduced in tunicamycin+4-PBA group (P<0.05). 4-PBA inhibited tunicamycin-induced decreases in both dendritic spine density and synaptic protein expression in the primary hippocampal neurons. 4-PBA attenuated tunicamycin-induced decrease in the cell viability. CONCLUSION:4-PBA not only attenuates ER stress of primary hippocampal neurons but also inhibits the decreases in both dendritic spine density and synaptic protein expression induced by tunicamycin. 相似文献
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AIM: To investigate the protective effects of sodium ferulate (SF) on apoptosis in cultured hippocampal neurons induced by sodium nitroprusside (SNP), and the effect of SF on expression of bcl-2 and bax. METHODS: The primary cultured hippocampal neurons were exposed to 50 μmol SNP, a nitric oxide-donor, for 24 h after pretreatment with different concentrations of SF (10-160 μmol/mL) for 6 h. Then neuronal viability was tested by MTT assay. Fluorescent staining with Hoechst 33258 and agarose gel electrophoresis was used to analyze apoptosis. The expressions of bcl-2, bax mRNA and protein were tested by RT-PCR and Western blotting. RESULTS: Pretreatment with SF(10-160 μmol/L) for 6 h increased the survival rate of neurons. SF prevented the neuronal nuclei from shrinkage, condensation and cleavage and blocked neuronal nuclear DNA fragmentation induced by SNP. SF also increased the expressions of bcl-2 mRNA and Bcl-2 protein and decreased the expressions of bax mRNA and Bax protein. CONCLUSION: SF prevents the cultured hippocampal neurons against SNP neurotoxicity. The mechanism of protection is related to the increase in Bcl-2 level and the decrease in Bax level. As a result, the ratio of Bcl-2/Bax is changed. 相似文献
3.
AIM:To establish a model of primary cultured neuron injury induced by D-galactose for the research in Alzheimer's disease. METHODS:Primary rat neurons cultured for 6 days were exposed to 50 mmol D-galactose for 72 h. The neural growth and neurite density were observed with HE stain and microscope, the neural metabolism rate and apoptosis rate were examined with MTT, immuno-enzyme assay and flow cytometry, respectively, and the aldose reductase mRNA expression was also detected with RT-PCR. RESULTS:The neural growth and development in neurons treated with D-galactose was retarded, the neural metabolism rate decreased from 0.762±0.030(n=33) to 0.543±0.064(n=11)(P<0.01 ), and the neural apoptosis rate in injured neurons increased from 0.060±0.029 (n=19) to 0.356±0.215(n=19), P<0.01. In addition, the neurite density in neurons treated with D-galactose decreased from 0.557±0.0422(n=10) to 0.468±0.0330(n=10)(P<0.01), the significant neural degeneration and necrosis were found. There is no aldose reductase mRNA expression in the neurons. CONCLUSION:A stable neuron injury model was established with 50 mmol/L D-galactose for 72 h, and it may be an useful tool for Alzheimer's disease research. 相似文献
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CAI Wei-bin YANG Zhong-han LI Chao-yang SONG Zhi-hong ZHOU Shi-hao LUO Xiao-feng GAO Guo-quan 《园艺学报》2005,21(4):652-656
AIM: To observe the effects of ginkgolide B on the neuron apoptosis induced by glutamate and explore whether this effects are related to the changes of calcium in neurons. METHODS: Primary neuron culture was prepared according to a previously reported procedure with slight modification. Neuron damage was induced by 0.8 mmol/L glutamate. The cell survival rate was examined by 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assays. The neuron morphological changes, Hoechst 33258 unclear-staining analysis and agarose gel electrophoresis of DNA were measured as the indexes of cell apoptosis. Intracellular free Ca2+ concentration in neurons was measured by using the fluorescent Ca2+ indicator Fura-2/AM. RESULTS: The cells, exposed to glutamate (0.8 mmol/L), showed characteristic change of apoptosis and calcium overload, which were relieved by the treatment of ginkgolide B (10-250 μmol/L), with survival increasing and cell morphology restoring and DNA fragment decreasing. CONCLUSIONS: Ginkgolide B prevents the neurons from glutamate neurotoxicity by inhibiting glutamate-induced apoptosis. The potential mechanism of its action may be related to the competitive PAF receptor binding of ginkgolide B and decreasing the intracellular calcium concentration in neurons. 相似文献
6.
AIM: To set up a glutamate-induced cell damage model in cultured hippocampal neurons, and to determine whether glutamate-induced neuronal apoptosis changes and whether this process is mediated by mitochondrial signal transduction pathways involving the release of cytochrome C. METHODS: Hippocampal neurons, isolated and cultured from new born Wistar rats, were exposed to various concentrations of glutamate. Extent of cell death was assessed by measuring the release of lactate dehydrogenase (LDH) in the culture media. Based on these data, an appropriate concentration of glutamate was selected, and all subsequent experiments were carried out under the concentration. Kinetics of glutamate-induced both apoptotic and necrotic cell death after exposure to glutamate for various times(3-24 h) were determined by flow cytometry and LDH release. The caspase-3 protein levels and cytochrome C release from mitochondria into cytosol in hippocampal neurons were determined by Western blotting. RESULTS: Glutamate treatment induced hippocampal neurons death in dose-dependent and time-dependent manners. A significant increase in LDH release (18.4%) was induced in the cells treated with 50 μmol/L glutamate, compared to control untreated cells(P<0.05). A significant increases in LDH release and apoptosis were observed at 6 h after glutamate treatment (P<0.05). The significant increase in the level of caspase-3 protein occurred at 3 h after glutamate exposure, which preceded neuronal cell apoptosis, and reached maximum levels at 6 h(62.4%). Treatment with glutamate induced a rapid release of cytochrome C into cytosol. Cytosolic cytochrome C showed a significant increase (P<0.05) as early as 30 min after glutamate treatment, which preceded the increase in caspase-3 level, and after 3 h, the level of cytochrome C was higher in the cytosol compared to the mitochondria. Concomitant with these changes in cytosol, the mitochondrial levels of cytochrome C decreased significantly. CONCLUSION: Exposure to 50 μmol/L glutamate induces apoptosis in cultured hippocampal neurons. The glutamate-induced apoptosis may be via the damage of mitochondria that results in cytochrome C release into cytosol, which activates caspase cascade and induces apoptotic cell death. 相似文献
7.
AIM: To explore the possible mechanism of tert-butyl hydroperoxide (t-BHP)-induced apoptosis in rat cortical neurons. METHODS: Primary cultured rat cortical neurons were performed in vitro and cell viability was measured by MTT assay. DNA fragmentation was used to evaluate cell apoptosis and mitochondrial transmembrane potential (ΔΨm) was determined by flow cytometric assay. Cellular glutathione (GSH) content was measured by spectrophotometer. Bcl-2 and Bax protein, cytosolic cytochrome c, cleaved caspase-3 and poly (ADP-ribose) polymerase (PARP) were detected by Western blotting. RESULTS: After exposure of cortical neurons to tBHP (25-400 μmol/L), the cell viability was reduced. ΔΨm and cellular GSH content were also decreased significantly. The level of Bcl-2 protein was reduced and Bax was elevated. Meanwhile, tBHP exposure resulted in cytochrome c release, caspase-3 and PARP proteolysis, DNA fragmentation and eventually neuron apoptosis. CONCLUSION: Mitochondrial damage may mediate tBHP- induced apoptosis in cortical neurons. 相似文献
8.
AIM: To observe the damage induced in the primary cultured rat cortical neurons by oxygen/glucose deprivation and reintroduction, and to investigate the neuroprotective mechanism of salvianolic acid B (SalB). METHODS: Primary cultured rat cortical neurons were randomly divided into the control group, the model group and the SalB group. The cell model was established by oxygen/glucose deprivation for 3 h followed oxygen/glucose reintroduction for 24 h. The cortical neurons viability was determined by MTT assay. The leakage rate of lactate dehydrogenase (LDH) was measured by chromatometry. The mitochondrial membrane potentials (MMP) and the apoptosis rate were quantitatively analyzed by flow cytometry. The cytosolic free calcium was assessed using LSCM. The morphologic changes of neuronal nuclei were observed by Hoechst 33342 fluorescence staining. RESULTS: Compared to the model group, the cortical neurons viability, the survival rate and the fluorescence value of MMP in the SalB group were obviously increased (P<0.05,P<0.01). In addition, in the SalB group, the leakage rate of LDH, the fluorescence intensity of cytosolic free calcium and the apoptosis rate were significantly lower than those in the model group (P<0.01). CONCLUSION: The neuroprotective mechanism of SalB in the oxygen/glucose deprivation and reintroduction neurons would be due to the fact that SalB maintains the MMP and the calcium homeostasis. 相似文献
9.
Protective effects of adenosine on cultured rat hippocampal neurons after oxygen-glucose deprivation
AIM:To investigate the protective effects of adenosine on cultured rat hippocampal neurons after oxygen-glucose deprivation.METHODS:The control and adenosine-treated hippocampal neurons cultured for 12 d were exposed to oxygen-glucose deprivation environment for 0.5-4 h and then cultured with original medium in normoxia for 24 h. The soma area, survival rate, effluxes of lactate dehydrogenase (LDH)and apoptosis of neurons were observed.RESULTS:The soma area, effluxes of lactate dehydrogenase from neurons and apoptosis were increased while survival rate of neurons was decreased after oxygen-glucose deprivation compared with those pre-oxygen-glucose deprivation. Compared with the control, after oxygen-glucose deprivation the soma area, effluxes of lactate dehydrogenase from neurons and apoptosis were decreased, however, the survival rate of neurons was increased in the adenosine group.CONCLUSION:Oxygen-glucose deprivation can lead to the severe damage of cultured hippocampal neurons, and adenosine can reduce neuronal injury induced by oxygen-glucose deprivation. 相似文献
10.
HUANG Cui-qin LI Qin FAN Chong-zhu GAN Dan-hui LI An ZHAO Jia-yi WANG Zhen LU Da-xiang 《园艺学报》2017,33(2):208-214
AIM: To investigate the protective effect of lycopene on primary mouse cerebrocortical neurons exposed to tert-butyl hydroperoxide (t-BHP) and its mechanisms of in vitro.METHODS: Primary cerebrocortical neurons of newborn C57 mice were extracted and divided into normal group, t-BHP group, lycopene+t-BHP group and lycopene group. The neuronal damage was induced by t-BHP exposure for 24 h, and the cell viability was examined by MTT assay. ROS content was measured by flow cytometry, and the protein levels of Bax, Bcl-2, caspase-3, cleaved caspase-3 and cytochrome C were examined by Western blot.RESULTS: The primary mouse cortical neurons expressed MAP-2 protein. Lycopene at concentration of 4 μmol/L reversed the decrease in cell viability. Flow cytometry revealed that lycopene treatment attenuated ROS content under the condition of t-BHP exposure. In addition, the protein level of Bcl-2 was increased, and the expression of Bax, cleaved caspase-3 and cytochrome-C was suppressed in lycopene+t-BHP group.CONCLUSION: The protective effect of lycopene on cortical neurons with t-BHP-induced injury may be involved in the mechanism of neuronal antioxidative response by down-regulating caspase-3 and Bax/Bcl-2 through the mitochondrial apoptotic pathway. 相似文献
11.
YUE Xiao-li LI Ping△ LIU Xin HUANG Qi-fu△ BARBIER-CHASSEFIERE Véronique MORIN Christophe PAPY-GARCIA Dulce 《园艺学报》2008,24(4):777-782
AIM: To verify the protection of astragalus polysaccharide (APS) on H2O2-stressed skin fibroblasts. METHODS: A model of acute H2O2 stress in primary skin fibroblast was used at concentration of 0.5 mmol/L by 30 min incubation. Dose responses of APS on cell survival was measured by MTT, cell death was evaluated by DAPI, and effect of APS on mitochondria, mitochondrial membrane potential and lysosome stabilization were measured by confocal microscopy. RESULTS: APS improved cell survival in a dose-dependent manner, starting at 0.5 mg/L and with a maximum at 1 mg/L. Moreover, APS inhibited mitochondrial membrane potential collapse, protected mitochondrial morphology and stablized lysosomal membrane. CONCLUSION: The results suggest the existence, at the mitochondria-lysosome level, of a new pathway of apoptotic regulation by APS. This might constitute a new therapeutic target where oxidative stress and lysosomal impairment are involved. 相似文献
12.
AIM:To study the relationship between cyclooxygenase 2(COX-2) and the damage of hippocampal neurons by aluminum overload in rats. METHODS:Newborn SD rats(less than 24 h) were used to establish the model of primary culture of hippocampal neurons. The neurons were treated with aluminum at concentration of 200 μmol/L. The techniques of RNA interference(RNAi) and cell transfection were used to study the role of COX-2 in hippocampal neuron. Following RNAi by cell transfection, Western blotting analysis was used to determine the protein expression of COX-2. Cell growth was assayed by the method of MTT. The pathological changes of the neurons were observed by fluorescence labeling. The activity of superoxide dismutase(SOD) and lactate dehydrogenase(LDH), and the content of malondialdehyde(MDA) were detected for evaluating cell damage. RESULTS:COX-2 RNAi by cell transfection significantly decreased the protein expression of COX-2 without changing the neuronal pathomorphology, cell viability, SOD activity and MDA content. However, it obviously improved livability and SOD activity of the hippocampal neurons, which were aluminum-overloaded. Inhibition of COX-2 expression also reduced the leakage of LDH and the content of MDA, and ameliorated the pathological changes in neurons. CONCLUSION:Moderate silence of COX-2 expression not only significantly affects the morphological changes and physiological functions of hippocampal neurons, but also prevents the neurons from aluminum-induced damages. 相似文献
13.
MENG Jing DING Xiao-yan ZHU Xiao-bo LIN Shao-fen GUO Meng-xiang TANG Shi-bo 《园艺学报》2009,25(11):2192-2196
AIM: To observe the effect of ginkgolide B (GB) on the intracellular calcium ion concentration (［Ca2+］i) and mitochondrial function of cultured rat retinal neurons in vitro.METHODS: in vitro primary culture of rat retinal neurons was used in the experiment. The apoptosis model of glutamate-induced retinal neurons was established and co-cultured with ginkgolide B. The ［Ca2+］i and mitochondrial membrane potential of the retinal neurons were detected by laser scanning confocal microscope.RESULTS: Glutamate decreased the survival rate of retinal neurons, increased the apoptosis and the ［Ca2+］i, lowered the mitochondrial membrane potential. The ［Ca2+］i was clearly diminished and the mitochondrial membrane potential was significantly increased with the GB intervention, and the apoptosis decreased significantly.CONCLUSION: GB protects retinal neurons from glutamate induced neurotoxicity. The effect of GB on retinal neurons might be due to its ability to decrease the ［Ca2+］i and increase mitochondrial membrane potential. 相似文献
14.
AIM and METHODS: The sodium ion Na+ and potassium ion K+ selective microelectrodes were used to measure changes of ionic activity of extracellular sodium and potassium( [Na+]o, [K+]o) in hippocampus and hippocampal slice during epieptic seizure induced by intrahippocampal microinjection of coriaria lactone(CL) in rats and perfusing hippocampal slice with CL. RESULTS:30 s, 1min and 2min after injection of CL into hippocampus, the [Na+]o decreased 27.7 mmol/L, 50.3 mmol/L, 57.8 mmol/L respectively and the [K+]o increased 2.3 mmol/L, 2.4 mmol/L, 2.9 mmol/L respectively compared with control values(P＜0.01). The [K+]o returned to the control level 3min after local application of CL, but the[Na+] o was still lower than that of control group(P＜0.01). The [Na+]o and the [K+]o were measured also in hippocampal silces and results are similar to those of experiments in vivo. CONCLUSION: The influx of Na+and the flux of K+occurred during epileptiform discharges of hippocampal neurons induced by administration of CL. 相似文献
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AIM: To investigate the role of high glucose in primary hepatocytes of mice fed with a high fat diet.METHODS: Male C57BL/6J mice were fed a high fat (45% of calories) diet ad libitum for 6 weeks to induce hepatic steatosis. Primary hepatocytes were isolated from the mouse liver by the 2 step collagenase perfusion method. The cells were incubated in low glucose (5 mmol/L), low glucose plus mannitol (30 mmol/L), or high glucose (35 mmol/L) DMEM medium for 12 h. The cell viability, apoptosis, mitochondrial membrane potential, and caspase enzymatic activities were measured. Furthermore, proteins related to the stress-sensitive signaling pathway of regulating high glucose-induced apoptosis in primary hepatocytes were determined by Western blotting.RESULTS: Incubation with 35 mmol/L glucose resulted in a significant decrease in cell viability and an increase in apoptosis, whereas mannitol had no significant effect on the cell viability or apoptosis. A progressive depolarization of the mitochondria, an increase in cytosol cytochrome C and a dramatic decrease in mitochondrial cytochrome C in high-glucose stressed hepatocytes were observed. The enzymatic activities of caspase-9 and caspase-3, but not caspase-8, were significantly increased in high glucose-stressed hepatocytes (P<0.05). High glucose treatment suppressed the expression of Bcl-2 and Bcl-xL, while it increased the expression of the pro-apoptotic factor Bax.CONCLUSION: High glucose stress reduces mitochondrial membrane potential, initiates mitochondria-mediated apoptotic pathways and promotes apoptosis of hepatocytes with steatosis. This may be an important pathological mechanism of hyperglycemia-induced progression of nonalcoholic fatty liver disease. 相似文献
16.
TANG Lu PEI Yue-hong ZHANG Nan LE Wei-dong FAN Dong-sheng DENG Min ZHANG Jun 《园艺学报》2009,25(12):2441-2446
AIM: To explore the mutual effect of co-culture of wild-type astrocytes (ASC) and motor neurons VSC4.1 (VSC) on the respective ability to produce reactive oxygen species (ROS). METHODS: The inhibition rates of cell growth in ASC and VSC in co-culture or independent culture was detected after exposed to excitatory stimulus by MTT method. Real-time observation of ROS production by ASC and VSC labeled with Hoechst 33342 was detected by confocal microscopy under the conditions of co-culture or independent culture. RESULTS: Higher concentration of glutamate induced a higher inhibition rate in mixed cell growth than that in ASC alone, while lower concentration of glutamate induced a higher inhibition rate in mixed cell growth than that in VSC only. Real-time observation by confocal microscopy showed that ROS production by VSC under the condition of co-culture, which showed a notable increase at 15 min, was significant less than that in independent culture, which peaked at 5 min and was gradually decreased. ROS production by ASC in co-culture began to increase significantly at 10 min. CONCLUSION: Compared to independent culture, ASC reduces the resting ROS production by co-cultured with VSC, while ASC prolongs the duration of ROS production by VSC after exposed to excitatory stimulus. 相似文献
17.
AIM: To observe the expression of apoptosis-related proteins in hippocampal neurons of ovariectomized (OVX) rats and explore the neuroprotective mechanism of the App17-mer peptide. METHODS: Female Wistar rats were randomly divided into three groups. Bilaterally ovariectomized rats with injection of App 17P peptide (3.5 μg in 0.1 mL/per rat, three times a week) formed the experimental group (17P+ OVX group). Anti-AIF, Bcl-2 and Bax antibodies were applied in the immunohistochemistry experiment. TUNEL was employed to detect apoptosis. RESULTS: The number of apoptotic neurons was clearly higher in hippocampal and cortex in OVX group than that in OVX+17P group. Immunohistochemistry demonstrated the increased expression of AIF, Bax in hippocampal neurons of OVX group. OVX group showed a significantly reduced expression of Bcl-2 in hippocampal neurons. Hippocampal tissue from OVX group showed the increased expression of AIF,Bax ,and showed diminished expression of Bcl-2 , treating with App17-mer peptide normalized the expression of these proteins. CONCLUSIONS: The expression of apoptosis-related proteins were abnormal in the OVX rats. App17-mer peptide normalized these changes ; Estrogen deficiency induced neuronal apoptosis. App17-mer peptide diminished apoptosis. 相似文献
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JIANG Xun ZENG Yao-ying HE Xian-hui XU Li-hui DI Jing-fang FENG Zheng ZHAO Jing-xian WANG Qing WANG Tong SHI Jian-bo 《园艺学报》2004,20(6):924-928
AIM: To investigate the effect of enhanced green fluorescence protein (EGFP) gene transfection on the cell cycle distribution of primary cultured human chondrocytes in order to establish a tracking method of cultured human nasoseptal chondrocytes. METHODS: pEGFP-N1 plasmid was amplified in E.coli, and purified by high purity kit. Primary cultured human chondrocytes,which were initially obtained from the nasoseptal cartilage, were cultured in vitro and transferred with pEGFP-N1 by means of electroporation with Amaxa nucleofector device. Transfering process and transient expression were evaluated by laser scanning confocal microscope (LSCM), the transfer efficiency and the cell cycle distribution were evaluated by flow cytometry. RESULTS: There was significant expression of EGFP at 24 h after transferring. The transfection efficiency of pEGFP-N1 into primary cultured human chondrocytes reached 35.37％ at 48 h. It didn't affect the process of cell adherance and had no effect on the cell cycle distribution. CONCLUSION: Primary cultured human chondrocytes, which were transfected with pEGFP, are alive in vitro, and the transferring process doesn't affect the cell cycle distribution. These results suggest that pEGFP-N1 is an ideal transient expression vector for primary cultured human chondrocytes and it might be a well tracer in construction tissue engineered cartilage. 相似文献
19.
ZHANG Jing-yuan ZHANG Yan-qiao ZHANG Yi-na PEI Li-chun XU Chang-qing YANG Wei 《园艺学报》2009,25(1):89-92
AIM: To observe the role of peroxysome proliferator activated receptor-γ (PPAR-γ) and the relationship of cyclooxygenase-2 (COX-2) and PPAR-γ in injury of cultured rat cortical neurons induced by hypoxia/reoxygenation. METHODS: Primary rat cortical neurons were cultured. Experiments include control group, hypoxia/ reoxygenation group and hypoxia/ reoxygenation with PPAR-γ agonist group. Cell viability was surveyed by MTT assay. COX-2 protein expression was measured by Western blotting.RESULTS: Neuron viability raised dramatically in hypoxia/reoxygenation with PPAR-γ agonist group, compared with hypoxia/reoxygenation group (P<0.05). The COX-2 protein expression in hypoxia/ reoxygenation with PPAR-γ agonist group decreased significantly compared with hypoxia/ reoxygenation group (P<0.05). CONCLUSION: PPAR-γ agonist inhibits the expression of COX-2 and reduces obviously cortical neuron injury induced by hypoxia/ reoxygenation. It may protect cortical neurons by down-regulating the expression of COX-2. 相似文献
20.
AIM: To establish the cell model of hippocampal neurons impaired by the supernatant of microglia conditioned medium (MCM) induced by LPS, and to study the mechanisms of neuron damage and the protection effect of curcumin. METHODS: The microglia were activated and stimulated by LPS at concentration of 5 μg/L. The supernatant of activated MCM was used to stimulate the hippocampal neurons. The morphology of the neurons was observed under light microscope and the survival rate was detected by MTT. The availability of respiration in the hippocampal neurons was determined by detecting the ratio of lactic acid/pyruvic acid, and the expression of 3 types of 1,4,5-inositol triphosphate (IP3R1, IP3R2, IP3R3) was detected by RT-PCR. RESULTS: The hippocampal neurons were damaged severely by the supernatant of activated MCM, and the morphology of the neurons changed significantly. Compared to control group, the ratio of lactic acid/pyruvic acid in MCM group was elevated and the expression levels of IP3R1 and IP3R3 in the hippocampal neurons were significantly increased. The ratio of lactic acid/pyruvic acid and the expression of IP3R1 in curcumin+MCM group were evidently lower than those in MCM group. However, no effect of curcumin on IP3R3 expression was observed, the changes of neural morphology was also ameliorated in curcumin+MCM group. CONCLUSION: Curcumin protects rat hippocampal neurons from damage induced by LPS-induced microglia condition medium． 相似文献