目的 运用网络药理学和分子对接技术研究羚珠散抗小儿易感病毒的有效成分和作用机制.方法 利用TCMID数据库查找羚珠散的化学成分,利用TCMSP、Pubchem、Swiss Target Prediction、SEA和STITCH数据获得羚珠散活性化合物的作用靶点;通过GeneCards数据库获得相关病毒性疾病靶点,取交集后得到共有靶点,即为羚珠散抗小儿易感病毒的潜在作用靶点.通过STRING数据库构建交集靶点的蛋白质相互作用(PPI)网络,基于degree值筛选重要靶点.利用DAVID平台对重要靶点进行基因本体论(GO)功能和京都基因与基因组百科全书(KEGG)通路富集分析.使用Cytoscape软件进行化合物–靶点网络拓扑分析,获得羚珠散抗小儿易感病毒的关键化合物和核心靶点.采用AutoDock Vina软件对筛选出的关键靶点和核心化合物进行分子对接验证.结果 共获得91个活性化合物以及184个药物–疾病交集靶点,经筛选获得羚珠散抗小儿易感病毒15个核心化合物(桉油烯醇、桉脂素、丁香烯、乙酸龙脑酯等)以及3个核心靶点[C反应蛋白(CRP)、趋化因子2(CCL2)、血红素加氧酶1(HMOX1)].KEGG通路富集分析结果显示,羚珠散抗小儿易感病毒可能主要通过调控肿瘤坏死因子(TNF)、Toll样受体、丝裂原活化蛋白激酶(MAPK)、叉头框蛋白O(FoxO)及T细胞受体等多种信号通路发挥治疗作用.分子对接结果表明,羚珠散抗易感病毒中10个核心化合物和核心靶点均有良好的结合能力,证明了网络药理学筛选结果的可靠性.结论 羚珠散可通过桉油烯醇、桉脂素、丁香烯、乙酸龙脑酯等主要活性成分,结合CRP、CCL2、HMOX1等核心靶点来调控机体多种炎症反应、免疫反应相关信号通路,从而发挥抗小儿易感病毒作用.

目的 探究天佛参口服液对人非小细胞肺癌A549细胞与裸鼠移植瘤增殖的作用以及相关作用机制.方法 采用Cell Titer-Glo发光法检测天佛参口服液对9种不同基因突变表型的肺癌细胞系增殖的抑制作用;采用流式细胞术检测天佛参口服液对A549细胞周期及凋亡的影响;采用Western blotting法考察天佛参口服液对A549细胞增殖相关蛋白表达的影响.裸鼠sc A549细胞建立裸鼠移植瘤模型,考察天佛参口服液对小鼠皮下移植瘤生长的影响.结果 天佛参口服液抑制A549细胞增殖,呈剂量相关性;天佛参口服液阻滞A549细胞周期于G0/G1期和G2/M期(P＜0.05、0.01),并且1％天佛参口服液可以显著诱导A549细胞凋亡(P＜0.01);天佛参口服液显著抑制表皮生长因子受体(epidermal growth factor receptor,EGFR)、Raf、丝裂原细胞外信号调节激酶(mitogen extracellular signal-regulated kinase,MEK)以及细胞外调节蛋白激酶(extracellular regulated protein kinase,ERK)蛋白的磷酸化水平(P＜0.05、0.01),呈剂量相关性.体内实验结果显示,2.25 mL/kg天佛参口服液对裸鼠移植瘤模型的肿瘤体内生长具有显著抑制作用(P＜0.05).结论 天佛参口服液对A549细胞的体内外生长具有显著抑制作用,其作用机制可能与抑制EGFR活性和下调Ras/Raf/MEK/ERK信号通路表达有关.

Objective To explore the mechanism of inhibitory effect of dimethyl sulfoxide (DMSO) on the hyperplasia of the fibrous capsule around the tissue expander. Methods The experimental model was established in rats as follows: after implanting the expander on the back of rats, 30 % DMSO or normal saline was injected into the expander. The former was classified as experimental group, and the latter as control group. The cystic wall was resected after the skin and soft tissues were expanded. In situ hybridization and the immunohistochemical staining were used to determine the expression of typesⅠand Ⅲ of collagen and procollagen mRNA in the cystic walls. Results It was found that both the typeⅠand Ⅲ of collagen content and the expressing quantity of mRNA of procollagen in the cystic wall of the experimental group were less than those of control group. Conclusion The results imply that the mechanism that DMSO inhibits the expression of typesⅠand Ⅲ of collagen in the fibrous cystic wall may be achieved through down-regulating the genetic expression of procollagen in the fibroblasts.