Objective: To observe the acting pattern on the immune system by Kidney tonifying (KT) drugs. Methods: Three composite recipes were used on the 7- and 14-day corticosterone rat model to study the effect of recipes on...Objective: To observe the acting pattern on the immune system by Kidney tonifying (KT) drugs. Methods: Three composite recipes were used on the 7- and 14-day corticosterone rat model to study the effect of recipes on the different patterns of immuno-modulatory and neuro- endocrinological systems. Results:The immune system of Spleen Invigorating(SI) group was well protected in either 7- or 14-day experiments,with the SI recipe showing no effect on the neuroendocrine system. It suggested that SI recipe might have direct action on immune system. On the other hand, KT group with no effect on neuroendocrine-immune (NEI) system in 7-day experiment, but showed a remarkable protective effect of the whole NEI system in 14-day experiment. Conclusion: The results indicated that KT recipe acts on the neuroendocrine system first, and then influence the immune system. It means that the action took place through down pathway of NEI network.展开更多
目的:运用网络药理学和分子对接的方法,探索健脾疏肝方治疗非酒精性脂肪性肝病(non-alcoholic fatty liver disease,NAFLD)的潜在机制。方法:利用中药系统药理学数据库与分析平台(traditional Chinese medicine systems pharmacology,TC...目的:运用网络药理学和分子对接的方法,探索健脾疏肝方治疗非酒精性脂肪性肝病(non-alcoholic fatty liver disease,NAFLD)的潜在机制。方法:利用中药系统药理学数据库与分析平台(traditional Chinese medicine systems pharmacology,TCMSP)和已发表的文献筛选健脾疏肝方的活性化合物和潜在作用靶点,利用人类基因数据库(GeneCards)、在线人类孟德尔遗传数据库(online mendelian inheritance in man,OMIM)和药物靶标数据库(therapeutic target database,TTD)筛选NAFLD的相关靶点,预测健脾疏肝方治疗NAFLD的潜在靶点。利用STRING数据库和Cytoscape软件构建共同靶标的PPI网络。利用DAVID数据库及微生信云平台进行基因本体(gene ontology,GO)和京都基因与基因组百科全书(kyoto encyclopedia of genes and genomes,KEGG)通路富集分析。最后利用AutoDock Vina和Pymol软件对核心靶点和主要活性化合物进行分子对接。结果:共筛选出117个活性化合物和279个潜在靶标,其中槲皮素(Quercetin)、木犀草素(luteolin)、豆甾醇(Stigmasterol)、山柰酚(kaempferol)为健脾疏肝方主要活性化合物。PPI网络显示白细胞介素6(interleukin-6,IL-6)、肿瘤坏死因子(tumor necrosis factor,TNF)、信号转换器和转录激活因子3(signal transducer and activator of transcription 3,STAT3)、前列腺素内过氧化物合酶2(prostaglandin-endoperoxide synthase 2,PTGS2)和血管内皮生长因子A(vascular endothelial growth factor,VEGFA)是关键靶蛋白。KEGG通路富集分析结果显示,癌症、TNF、乙型病毒性肝炎、MAPK、PI3K-Akt及NAFLD信号通路可能是健脾疏肝方干预NAFLD的潜在机制。分子对接结果表明,健脾疏肝方主要活性化合物与核心靶标具有良好的结合能力。结论:健脾疏肝方可以通过多组分、多靶点及多通路起到干预NAFLD的作用。展开更多
目的:探讨补肾健脾活血方对过表达分泌型卷曲相关蛋白1(secreted frizzled related protein 1,SFRP1)、沉默SFRP1的UMR106细胞成骨分化及雌激素受体α(estrogen receptorα,ERα)的影响。方法:通过构建SFRP1过表达及沉默重组腺病毒载体...目的:探讨补肾健脾活血方对过表达分泌型卷曲相关蛋白1(secreted frizzled related protein 1,SFRP1)、沉默SFRP1的UMR106细胞成骨分化及雌激素受体α(estrogen receptorα,ERα)的影响。方法:通过构建SFRP1过表达及沉默重组腺病毒载体,并转染大鼠类成骨细胞系UMR106细胞,初步分为空载腺病毒组、过表达SFRP1组、沉默SFRP1组,并根据含药血清和生理盐水(空白)血清干预的不同分为6组,观察6组细胞的碱性磷酸酶(alkaline phosphatase,ALP)活性及细胞ERα蛋白表达情况。结果:含药血清干预的空载腺病毒组、SFRP1沉默组及SFRP1过表达组72 h后UMR106细胞ALP活性和ERα蛋白表达均高于空白血清干预的空载腺病毒组、SFRP1沉默组及SFRP1过表达组(P<0.05);空白血清+SFRP1沉默组的UMR106细胞ALP活性及ERα蛋白表达高于空白血清+空载腺病毒组(P<0.05),而空白血清+SFRP1过表达组的UMR106细胞ALP活性及ERα蛋白表达低于空白血清+空载腺病毒组(P<0.05)。结论:过表达SFRP1可以抑制UMR106细胞成骨分化,并下调ERα蛋白表达;沉默SFRP1和补肾健脾活血方均可促进UMR106细胞成骨分化,并上调ERα蛋白表达,且两者共同干预时作用更显著,说明补肾健脾活血方能够抑制SFRP1表达,而SFRP1并不是补肾健脾活血方调节成骨细胞代谢,提高成骨分化活性和促进ERα蛋白表达的唯一靶点,可能存在其他靶点共同促进调节成骨细胞代谢。展开更多
文摘Objective: To observe the acting pattern on the immune system by Kidney tonifying (KT) drugs. Methods: Three composite recipes were used on the 7- and 14-day corticosterone rat model to study the effect of recipes on the different patterns of immuno-modulatory and neuro- endocrinological systems. Results:The immune system of Spleen Invigorating(SI) group was well protected in either 7- or 14-day experiments,with the SI recipe showing no effect on the neuroendocrine system. It suggested that SI recipe might have direct action on immune system. On the other hand, KT group with no effect on neuroendocrine-immune (NEI) system in 7-day experiment, but showed a remarkable protective effect of the whole NEI system in 14-day experiment. Conclusion: The results indicated that KT recipe acts on the neuroendocrine system first, and then influence the immune system. It means that the action took place through down pathway of NEI network.
文摘目的:运用网络药理学和分子对接的方法,探索健脾疏肝方治疗非酒精性脂肪性肝病(non-alcoholic fatty liver disease,NAFLD)的潜在机制。方法:利用中药系统药理学数据库与分析平台(traditional Chinese medicine systems pharmacology,TCMSP)和已发表的文献筛选健脾疏肝方的活性化合物和潜在作用靶点,利用人类基因数据库(GeneCards)、在线人类孟德尔遗传数据库(online mendelian inheritance in man,OMIM)和药物靶标数据库(therapeutic target database,TTD)筛选NAFLD的相关靶点,预测健脾疏肝方治疗NAFLD的潜在靶点。利用STRING数据库和Cytoscape软件构建共同靶标的PPI网络。利用DAVID数据库及微生信云平台进行基因本体(gene ontology,GO)和京都基因与基因组百科全书(kyoto encyclopedia of genes and genomes,KEGG)通路富集分析。最后利用AutoDock Vina和Pymol软件对核心靶点和主要活性化合物进行分子对接。结果:共筛选出117个活性化合物和279个潜在靶标,其中槲皮素(Quercetin)、木犀草素(luteolin)、豆甾醇(Stigmasterol)、山柰酚(kaempferol)为健脾疏肝方主要活性化合物。PPI网络显示白细胞介素6(interleukin-6,IL-6)、肿瘤坏死因子(tumor necrosis factor,TNF)、信号转换器和转录激活因子3(signal transducer and activator of transcription 3,STAT3)、前列腺素内过氧化物合酶2(prostaglandin-endoperoxide synthase 2,PTGS2)和血管内皮生长因子A(vascular endothelial growth factor,VEGFA)是关键靶蛋白。KEGG通路富集分析结果显示,癌症、TNF、乙型病毒性肝炎、MAPK、PI3K-Akt及NAFLD信号通路可能是健脾疏肝方干预NAFLD的潜在机制。分子对接结果表明,健脾疏肝方主要活性化合物与核心靶标具有良好的结合能力。结论:健脾疏肝方可以通过多组分、多靶点及多通路起到干预NAFLD的作用。
文摘目的:探讨补肾健脾活血方对过表达分泌型卷曲相关蛋白1(secreted frizzled related protein 1,SFRP1)、沉默SFRP1的UMR106细胞成骨分化及雌激素受体α(estrogen receptorα,ERα)的影响。方法:通过构建SFRP1过表达及沉默重组腺病毒载体,并转染大鼠类成骨细胞系UMR106细胞,初步分为空载腺病毒组、过表达SFRP1组、沉默SFRP1组,并根据含药血清和生理盐水(空白)血清干预的不同分为6组,观察6组细胞的碱性磷酸酶(alkaline phosphatase,ALP)活性及细胞ERα蛋白表达情况。结果:含药血清干预的空载腺病毒组、SFRP1沉默组及SFRP1过表达组72 h后UMR106细胞ALP活性和ERα蛋白表达均高于空白血清干预的空载腺病毒组、SFRP1沉默组及SFRP1过表达组(P<0.05);空白血清+SFRP1沉默组的UMR106细胞ALP活性及ERα蛋白表达高于空白血清+空载腺病毒组(P<0.05),而空白血清+SFRP1过表达组的UMR106细胞ALP活性及ERα蛋白表达低于空白血清+空载腺病毒组(P<0.05)。结论:过表达SFRP1可以抑制UMR106细胞成骨分化,并下调ERα蛋白表达;沉默SFRP1和补肾健脾活血方均可促进UMR106细胞成骨分化,并上调ERα蛋白表达,且两者共同干预时作用更显著,说明补肾健脾活血方能够抑制SFRP1表达,而SFRP1并不是补肾健脾活血方调节成骨细胞代谢,提高成骨分化活性和促进ERα蛋白表达的唯一靶点,可能存在其他靶点共同促进调节成骨细胞代谢。
