Effect of Tiantai No.1 (天泰1号) on β-amyloid-induced neurotoxicity and NF-κ B and cAMP responsive element-binding protein

Objective： To investigate the effect and molecular mechanism of Tiantai No.1 （天泰1号）, a compound Chinese herbal preparation, for the prevention and reduction of neurotoxicity induced by betaamyloid peptides （Abeta） in vitro and its effects on nuclear factor-κB （NF-κB） and cAMP responsive element-binding protein （CREB） pathways using the gene transfection technique. Methods： B104 neuronal cells were used to examine the effects of Tiantai No.1 on lowering the neurotoxicity induced by Abeta. The cells were pre-treated with Tiantai No.1 at doses of 50, 100,150, or 200μg/mL respectively for 3 days and co-treated with Tiantai No.1 and beta-amyloid peptidel-40 （Aβ 1-40, 10 μmol/L） for 48 h or post-treated with Tiantai No.1 for 48 h after the cells were exposed to beta-amyloid peptides25-35 （Aβ 25-35） for 8 h. In gene transfection assays, cells were treated with Tiantai No.1 at 50 μg/mL and 150μg/mL for 5 days or co-treated with Tiantai No.1 and A 13 1-40 （5 μmo/L） for 3 days after electroporation for the evaluation of NF- κB and CREB expression. Results： Pre-treating and co-treating B104 neuronal cells with Tiantai No.1 lowered the neurotoxicity induced by Abeta, and post-treating with Tiantai No.1 reduced or blocked B104 neuronal apoptotic death induced by Abeta （P〈0.05, P〈0.01）. With a dose-dependent relationship, the same treatments increased the expression of NF-κB or CREB in B104 neuronal cells （P〈0.05, P〈0.01）. Meanwhile, Tiantai No.1 reduced Aβ-40 induced inhibition on NF-κB expression （P〈0.01）. Conclusions： Tiantai No.1 can protect neurons against the neurotoxicity induced by Abeta. The neuroprotective mechanisms may be associated with the activation of NF-κB and cAMP cellular signal pathways.     

Effect of Tiantai No.1(天泰1号)on Gene Expression Profiles in Hippocampus of Alzheimer's Disease Rats by Bioinformatic Analysis

Objective:To study the effect of Tiantai No.1(天泰1号) on gene expression profile in hippocampus of Alzheimer's disease(AD) rat,molecular genetic target points of the effect of this drug were defined,its molecular genetic pharmacodynamic mechanism of anti-AD was further explored at molecular gene level,and a scientific basis was provided for its clinical availability and promotion.Methods:Thirty male SpragueDawley rats were divided into three groups with 10 rats per group:sham-operation group,model group and Tiantai No.1 group.Sterile surgical procedure was applied,the model group with bilateral hippocampal injection of Aβ_(1-40) was established,and normal saline was used instead of Aβ_(1-40)in the sham-operation group.One week after the models was made,rats were administered by gastric lavage once every day for three consecutive weeks.The rats of the sham-operation group and the model group were daily fed with purified water by lavage;the rats of the Tiantai No.1 group treated group were administered with Tiantai No.1 by lavage.Total RNAs of hippocampus tissues were extracted with Trizol,the changes of hippocampus gene expression profiles in the above three groups were analyzed by using Affymetrix rat whole genome expression profile microarray.Results:Microarray analysis showed that,compared with the sham-operation group,the hippocampus of the model group had 50 up-regulated genes with significant difference(fold change 2),and 21 down-regulated genes with significant difference(fold change 0.5);compared with the hippocampus of the model group,the hippocampus of the Tiantai No.1 group was found to have 5 up-regulated genes with significant difference(fold change 2) and 20down-regulated genes with significant difference(fold change 0.5).The functions of differentially expressed genes of the groups were involved in nervous system's development,neuronic differentiation and function-regulation,cellular growth and differentiation and apoptosis,synaptic occurrence and plasticity,inflammation and immune response,ion channels/transporters,cellular signal transduction,cellular material/energy metabolism and so on.Conclusion:Tiantai No.1 can regulate hippocampal function,and further regulate the brain function of animals in multiple gene target points by a number of ways.     

Effect of Tiantai No.1(天泰1号) on β-Amyloid-induced Neurotoxicity and NF- к B and cAMP Responsive Element-binding Protein

To investigate the effect and molecular mechanism of Tiantai No.1 (天泰1号), a compound Chinese herbal preparation, for the prevention and reduction of neurotoxicity induced by beta-element-binding protein (CREB) pathways using the gene transfection technique. Methods: B104 neuronal cells were used to examine the effects of Tiantai No.1 on lowering the neurotoxicity induced by Abeta. The cells were pre-treated with Tiantai No.1 at doses of 50, 100, 150, or 200 μg/mL respectively for 3 days and co-treated with Tiantai No.1 and beta-amyloid peptidel-40 (Aβ 1-40, 10 μmol/L) for 48 h or post-treated with Tiantai No.1 for 48 h after the cells were exposed to beta-amyloid peptides25-35 (A β 25-35) for 8 h. In gene transfection assays, cells were treated with Tiantai No.1 at 50 μg/m/and 150 μg/mL for 5 days or co-treated with Tiantai No.1 and A β 1-40 (5 μ mo/L) for 3 days after electroporation for the with Tiantai No.1 lowered the neurotoxicity induced by Abeta, and post-treating with Tiantai No.1 reduced or blocked B104 neuronal apoptotic death induced by Abeta (P相似文献   

Effect of Jieze No.1 (洁泽 号) on cervicitis caused by ureaplasma urealyticum and on ureaplasma urealyticum in vitro

Objective： To observe the clinical therapeutic effect of Jieze No. 1 （洁泽Ⅰ号） on cervicitis caused by ureaplasma urealyticum and its inhibitory effect on ureaplasma urealyticum （Uu） in vitro. Methods： A total of 393 patients suffering from cervicitis induced by ureaplasma urealyticum without other complications were randomly assigned to 3 groups, the combined treatment group： 140 patients treated with Chinese herbs Jieze No.1 by vaginal lavage, 30 min each time, once a clay for 10 consecutive clays and oral administration of Azithromycin, 1.0 g once every 72 h for three times; Jieze group： 115 patients were treated with Jieze No.1 alone by vaginal lavage, 30 min each time, once a day for 10 consecutive days; and the Azithromycin group： 138 patients were treated with oral administration of Azithromycin, 1.0 g once in 72 h for three times. All the patients were treated for 1 therapeutic course and condom were used for contraception during the treatment course. The Uu patients were examined again after 21 clays of treatment. The therapeutic effect on cervicitis was observed. The experimental study of Jieze No. 1 on the Uu strain separated from the secretion of the urogenital tract was also observed. The minimum inhibitory concentration （MIC） and minimum bactericidal concentration （MBC） of the Uu were investigated. Results： The total effective rate of the combined group was 85.3%, showing a significant difference compared with the Jieze group （67.8%） and the Azithromycin group （60.3%, both P〈0.01）. There was no statistical significance between the latter two groups （P〉0.05）. The clearing rate of Uu in the combined group was 78.4%, that of the Jieze group was 60.9% and the Azithromycin group was 47.9%. The combined group also showed a significant difference in comparison with the other two groups （all P〈0.01）. Especially for the drugresistant strain, the clearing rate of Uu reached 48.1% in the combined group, 42.1% in the Jieze group, and 16.1% in the Azithromyc     

Qushi Huayu Decoction (祛湿化瘀方) Inhibits Protein and Gene Expression of Cathepsin B in HepG2 Cells Induced by Free Fatty Acids

Objective: To study the experimental efficacy of Qushi Huayu Decoction (祛湿化瘀方,QHD) on protein and gene expression of cathepsin B (ctsb) in HepG2 cells induced by free fatty acids (FFAs).Methods: The model of HepG2 steatosis and tumor necrosis factor-α (TNF-α) secretion was induced by long-chain FFAs.HepG2 cells were divided into 4 groups: control group (group C),model group (group M),low-dose QHD group (group L) and high-dose QHD group (group H ).Long-chain FFAs were added to groups M,L and H.The 10% blank-control serum was added to group C and M,while 5% and 10% QHD-containing sera were added to group L and H,respectively.The levels of serum TNF-α and cellular triglyceride (TG) were detected.Cellular p-IκB and ctsb expression were detected using Western blot and PCR.The expression and distribution of ctsb were observed by immunofluorescence.Results: After incubating with FFA for 24 h,TG deposition in HepG2,TNF-α content in cell supernatant,the protein expression of cellular ctsb and P-IκB,as well as mRNA expression of ctsb increased markedly in group M compared with group C (P0.05,P0.01).Compared with group M,TG deposition,the expression of cellular ctsb,P-IκB and ctsb mRNA in groups L and H,as well as TNF-α content in group H,decreased significantly (P0.05).Cell immunochemical fluorescence studies showed that ctsb was released from lysosomes and distributed in the cytoplasm extensively and diffusedly after being stimulated with FFA.In this study,these above-mentioned changes were inhibited markedly in groups L and H.Conclusion: QHD might have a direct inhibitory effect on the ctsb target in the FFA-ctsb-TNFα pathway of hepatic lipotoxicity.