|
|
|
题名
|
作者
|
年代
|
出处
|
被引量
|
| 1 | Effect of rifampicin pre-and post-treatment on rotenone-induced dopaminergic neuronal apoptosis and alpha-synuclein expression显示文摘BACKGROUND: Rifampicin inhibits the formation of α-synuclein multimer and protects against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyritine (MPTP)-induced PC12 cell apoptosis.OBJECTIVE: To compare the effect of rifampicin pre-and post-treatment on tyrosine hydroxylase and α-synuclein expression in substantia nigra pars compacta in a rat model of Parkinson’s disease.DESIGN,TIME AND SETTING: A randomized,controlled experiment was performed at the Experimental Animal Center of Sun Yat-sen University North Campus (China) from November 2006 to October 2008.MATERIALS: Rifampicin was purchased from MD,USA;rotenone was purchased from Sigma,USA;mouse anti-rat α-synuclein monoclonal antibody was purchased from B&D,USA;and rabbit anti-rat tyrosine hydroxylase monoclonal antibody was purchased from Chemicon,USA.METHODS: A total of 72 male,Sprague Dawley rats,aged 8 weeks,were randomly assigned to 5 groups: blank control (n = 12),rifampicin (n = 12),rotenone (n = 16),rifampicin pre-treatment (n = 16),and rifampicin post-treatment (n = 16).Parkinson’s disease model rats were established via a subcutaneous injection of rotenone (1.5 mg/kg per day) in the three treatment groups,once a day for 3 successive weeks.Rifampicin (30 mg/kg per day) was intragastrically administered in the rifampicin pre-treatment group 3 days prior to rotenone induction and in the rifampicin post-treatment group 7 days after rotenone induction.Rats were treated with a subcutaneous injection of 1 mL/kg per day sunflower oil in the blank control group and an intragastric injection of 30 mg/kg per day rifampicin in the rifampicin group,once a day for 3 successive weeks in total.MAIN OUTCOME MEASURES: Prior to treatment and in the end of the 3rd week after treatment,the rats were evaluated using the modified neurological severity score.The substantia nigra from the rats was extracted for hematoxylin-eosin staining.Western blot analysis was performed to determine tyrosine hydroxylase and α-synuclein expression.RESULTS: Hematoxylin-eosin staining revealed a significant reduction in the number of substantia nigral neurons in the rotenone group,in addition to neurodegradation,hypopigmentation,and pyknosis.In the rifampicin pre-treatment and post-treatment groups,the number of dopaminergic neurons was significantly increased compared with the rotenone group (P < 0.01),with slight neuronal damage.Compared with the rotenone group,substantia nigral tyrosine hydroxylase expres-sion was significantly increased in the rifampicin pre-treatment and post-treatment groups (P < 0.01),but α-synuclein expression and modified neurological severity scores were significantly decreased (P < 0.01).In addition,the effect of rifampicin in the pre-treatment group was superior to the post-treatment group.There was no significant difference in tyrosine hydroxylase and α-synuclein expression,or in the modified neurological severity scores,between the blank control and rifampicin groups (P > 0.05).CONCLUSION: Rifampicin significantly attenuated neuropathological and behavioral motor deficits induced by rotenone.Moreover,rifampicin enhanced tyrosine hydroxylase expression,but inhibited α-synuclein expression.The effect of rifampicin pre-treatment was superior to rifampicin post-treatment. | Yuanlin Sun Guohua Zhang Jie Xu Shiwen Chen Enxiang Tao Changqing Xu M. Catherine Bennett | 2010 | Neural Regeneration Research2010，5，2： | 4 |
| 2 | Rifampicin inhibits apoptosis in rotenone-induced differentiated PC12 cells by ameliorating mitochondrial oxidative stress显示文摘BACKGROUND:Previous studies have shown that rifampicin exhibits neuroprotective effects,but the precise mechanisms remain unclear.Rifampicin is thought to exert the neuroprotective effect as a hydroxyl free radical scavenger.OBJECTIVE:To investigate the protective effects of rifampicin pretreatment on rotenone-induced mitochondrial oxidative stress in differentiated PC12 cells.DESIGN,TIME AND SETTING:A repeated measure,cell-based study was performed at the Department of Neurology,Second Affiliated Hospital,Sun Yat-sen University,China between December 2007 and November 2008.MATERIALS:PC12 cells were a kind gift from the Physiology Laboratory of Zhongshan Medical School,Sun Yat-sen University,China.Rotenone and rifampicin were purchased from Sigma,USA.METHODS:PC12 cells were differentiated by culturing with 100 ng/mL 7S nerve growth factor for 9 days in Dulbecco's modified Eagle's medium/Nutrient Mix F12(DMEM/F12) supplemented with 10% fetal bovine serum.The cells were assigned to six groups according to various treatment conditions:control,cultured with normal media;rifampicin group,treated with 300 μmol/L rotenone for 26 hours;rotenone group,treated with 2.5 μmol/L rotenone for 24 hours;rifampicin pretreatment groups,pretreated with 100,200,and 300 μmol/L rifampicin for 2 hours,respectively,followed by 2.5 μmol/L rotenone for 24 hours.MAIN OUTCOME MEASURES:Mitochondrial membrane potential was measured by fluorescence microscopy and flow cytometry,respectively,using rhodamine123 staining.Intracellular reactive oxygen species formation was analyzed by flow cytometry using 2',7'-dichlorofluorescin-diacetate staining,and intracellular reduced glutathione was measured with a microplate reader.Cell viability was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay.Cell apoptosis was detected by Hoechst 33342 staining and flow cytometry.RESULTS:Increased apoptosis in rotenone-induced,differentiated,PC12 cells was accompanied by the loss of mitochondrial transmembrane potential,the formation of reactive oxygen species,and reduced glutathione depletion(P<0.01).Rotenone-induced mitochondrial dysfunction was blocked in a dose-dependent manner by rifampicin(P<0.05 or P<0.01).CONCLUSION:Pretreatment of differentiated PC12 cells with rifampicin blocked rotenone-induced apoptosis by ameliorating mitochondrial dysfunction and oxidative stress. | Shiwen Chen Yuanlin Sun Zhifeng Zeng Enxiang Tao | 2010 | Neural Regeneration Research2010，5，4： | 2 |
| 3 | Paroxetine engenders analgesic effects through inhibition of p38 phosphorylation in a rat migraine model显示文摘In this study,a model of migraine was established by electrical stimulation of the superior sagittal sinus in rats.These rats were then treated orally with paroxetine at doses of 2.5,5,or 10 mg/kg per day for 14 days.Following treatment,mechanical withdrawal thresholds were significantly higher,extracellular concentrations of 5-hydroxytryptamine in the periaqueductal grey matter and nucleus reticularis gigantocellularis were higher,and the expression of phosphorylated p38 in the trigeminal nucleus caudalis was lower.Our experimental findings suggest that paroxetine has analgesic effects in a rat migraine model,which are mediated by inhibition of p38 phosphorylation. | Chuanming Wang Wei Bi Yanran Liang Xiuna Jing Songhua Xiao Yannan Fang Qiaoyun Shi Enxiang Tao | 2012 | Neural Regeneration Research2012，7，13： | 2 |
| 4 | Delivery of cationic polymer-siRNA nanoparticles for gene therapies in neural regeneration显示文摘 | Yanran Liang Zhonglin Liu Xintao Shuai Weiwei Wang Jun Liu Wei Bi Chuanming Wang Xiuna Jing Yunyun Liu Enxiang Tao | 2012 | Biochemical and Biophysical Research Communications2012，，4： | 1 |
| 5 | Neuron-specific enolase expression in a rat model of radiation-induced brain injury following vascular endothelial growth factor-modified neural stem cell transplantation显示文摘<正>BACKGROUND:Previous studies have shown that transplantation of vascular endothelial growth factor(VEGF)-modified neural stem cells(NSC) provides better outcomes,compared with neural stem cells,in the treatment of brain damage. OBJECTIVE:To compare the effects of VEGF-modified NSC transplantation and NSC transplantation on radiation-induced brain injury,and to determine neuron-specific enolase(NSE) expression in the brain. DESIGN,TIME,AND SETTING:The randomized,controlled study was performed at the Linbaixin Experimental Center,Second Affiliated Hospital,Sun Yat-sen University,China from November 2007 to October 2008. MATERIALS:VEGF-modified C17.2 NSCs were supplied by Harvard Medical School,USA. Streptavidin-biotin-peroxidase-complex kit(Boster,China) and 5,6-carboxyfluorescein diacetate succinimidyl ester(Fluka,USA) were used in this study. METHODS:A total of 84 Sprague Dawley rats were randomly assigned to a blank control group(n = 20),model group(n = 20),NSC group(n = 20),and a VEGF-modified NSC group(n = 24).Rat models of radiation-induced brain injury were established in the model,NSC,and VEGF-modified NSC groups.At 1 week following model induction,10μL(5×10~4 cells/μL) VEGF-modified NSCs or NSCs were respectively infused into the striatum and cerebral cortex of rats from the VEGF-modified NSC and NSC groups.A total of 10μL saline was injected into rats from the blank control and model groups. MAIN OUTCOME MEASURES:NSE expression in the brain was detected by immunohistochemistry following VEGF-modified NSC transplantation. RESULTS:NSE expression was significantly decreased in the brains of radiation-induced brain injury rats(P<0.05).The number of NSE-positive neurons significantly increased in the NSC and VEGF-modified NSC groups,compared with the model group(P<0.05).NSE expression significantly increased in the VEGF-modified NSC group,compared with the NSC group,at 6 weeks following transplantation(P<0.05). CONCLUSION:VEGF-modified NSC transplantation increased NSE expression in rats with radiation-induced brain injury,and the outcomes were superior to NSC transplantation. | Songhua Xiao Chaohui Duan Qingyu Shen Yigang Xing Ying Peng Enxiang Tao Jun Liu | 2009 | Neural Regeneration Research2009，4，10： | 1 |
您所在的机构暂未开通此部分的功能，请联系管理员