AIM: To investigate whether troglitazone (TGZ), theperoxisome proliferator-activated receptor (PPAR) gammaligand, can induce apoptosis and inhibit cell proliferation inhuman liver cancer cell line HepG2 and to explore...AIM: To investigate whether troglitazone (TGZ), theperoxisome proliferator-activated receptor (PPAR) gammaligand, can induce apoptosis and inhibit cell proliferation inhuman liver cancer cell line HepG2 and to explore themolecular mechanisms.
METHODS: [3-(4,5)-dimethyithiazol-2-yl]-2,5-diphenyltetrazolium bromide (NTT), [3H] Thymidine incorporation,Hochest33258 staining, DNA ladder, enzyme-linkedimmunosorbent assay (ELISA), RT-PCR, Northern and Western blotting analyses were employed to investigate the effect of TGZ on HepG2 cells and related molecular mechanisms.RESULTS: TGZ was found to inhibit the growth of HepG2cells and to induce apoptosis. During the process, the expression of COX-2 mRNA and protein and Bcl-2 protein was down-regulated, while that of Bax and Bak proteins was up-regulated, and the activity of caspase-3 was elevated.Furthermore, the level of PGE2 was decreased transiently after 12 h of treatment with 30 gM troglitazone.
CONCLUSION: TGZ inhibits cell proliferation and induces apoptosis in HepG2 cells, which may be associated with the activation of caspase-3-like proteases, down-regulation of the expression of COX-2 mRNA and protein, Bcl-2 protein,the elevation of PGE2 levels, and up-regulation of the expressions of Bax and Bak proteins.展开更多
目的：应用蛋白质组学方法深入地研究含有嗜酸乳杆菌、乳双歧杆菌和低聚木糖的合生元制剂通过调节自发性高血压大鼠肠道菌群实现降血压的机制,为临床治疗高血压提供新的途径,为研究高血压病理生理机制提供新的思路。方法：选取6周龄、雄...目的：应用蛋白质组学方法深入地研究含有嗜酸乳杆菌、乳双歧杆菌和低聚木糖的合生元制剂通过调节自发性高血压大鼠肠道菌群实现降血压的机制,为临床治疗高血压提供新的途径,为研究高血压病理生理机制提供新的思路。方法：选取6周龄、雄性7只WKY大鼠和14只SHR大鼠分为对照组、模型组和给药组。给药组每只受试大鼠灌胃给予合生元制剂,7周后分离回肠段,提取并纯化蛋白,采用iTRAQ技术标记肽段,并通过LC-MS/MS分析这些差异表达的蛋白质。用Protein Pilot 4.5软件定性鉴别,并通过STRING进行分析以显示它们的注释和KEGG途径富集。结果：蛋白质组学和免疫组织化学结果显示,6种与PPAR信号途径有关的差异表达蛋白在治疗组回肠中被重新调节,PPARβ和PPARγ显着上调,表明PPARβ和PPARγ信号通路参与合生元降压机制。结论：合生元能通过改变肠道微生物结构,调节PPAR信号通路,激活PPARβ和PPARγ在回肠节段的级联反应,从而改善血压。展开更多
文摘AIM: To investigate whether troglitazone (TGZ), theperoxisome proliferator-activated receptor (PPAR) gammaligand, can induce apoptosis and inhibit cell proliferation inhuman liver cancer cell line HepG2 and to explore themolecular mechanisms.
METHODS: [3-(4,5)-dimethyithiazol-2-yl]-2,5-diphenyltetrazolium bromide (NTT), [3H] Thymidine incorporation,Hochest33258 staining, DNA ladder, enzyme-linkedimmunosorbent assay (ELISA), RT-PCR, Northern and Western blotting analyses were employed to investigate the effect of TGZ on HepG2 cells and related molecular mechanisms.RESULTS: TGZ was found to inhibit the growth of HepG2cells and to induce apoptosis. During the process, the expression of COX-2 mRNA and protein and Bcl-2 protein was down-regulated, while that of Bax and Bak proteins was up-regulated, and the activity of caspase-3 was elevated.Furthermore, the level of PGE2 was decreased transiently after 12 h of treatment with 30 gM troglitazone.
CONCLUSION: TGZ inhibits cell proliferation and induces apoptosis in HepG2 cells, which may be associated with the activation of caspase-3-like proteases, down-regulation of the expression of COX-2 mRNA and protein, Bcl-2 protein,the elevation of PGE2 levels, and up-regulation of the expressions of Bax and Bak proteins.
文摘目的：应用蛋白质组学方法深入地研究含有嗜酸乳杆菌、乳双歧杆菌和低聚木糖的合生元制剂通过调节自发性高血压大鼠肠道菌群实现降血压的机制,为临床治疗高血压提供新的途径,为研究高血压病理生理机制提供新的思路。方法：选取6周龄、雄性7只WKY大鼠和14只SHR大鼠分为对照组、模型组和给药组。给药组每只受试大鼠灌胃给予合生元制剂,7周后分离回肠段,提取并纯化蛋白,采用iTRAQ技术标记肽段,并通过LC-MS/MS分析这些差异表达的蛋白质。用Protein Pilot 4.5软件定性鉴别,并通过STRING进行分析以显示它们的注释和KEGG途径富集。结果：蛋白质组学和免疫组织化学结果显示,6种与PPAR信号途径有关的差异表达蛋白在治疗组回肠中被重新调节,PPARβ和PPARγ显着上调,表明PPARβ和PPARγ信号通路参与合生元降压机制。结论：合生元能通过改变肠道微生物结构,调节PPAR信号通路,激活PPARβ和PPARγ在回肠节段的级联反应,从而改善血压。
