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Anti-cancer activity of Tonglian decoction against esophageal cancer cell proliferation through regulation of the cell cycle and PI3K/Akt signaling pathway
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作者 yongsen jia Lijuan Qin +4 位作者 Chunhua jiang Qing Lin Fuling Tian Huijuan Cao Xin Yan 《Journal of Traditional Chinese Medical Sciences》 2015年第2期120-126,共7页
Objective:The purpose of this study was to observe the anti-cancer activity of Tonglian decoction(TD)on esophageal cancer(EC)cells in vitro,and to elucidate the related molecular mechanisms in the cell cycle and PI3K/... Objective:The purpose of this study was to observe the anti-cancer activity of Tonglian decoction(TD)on esophageal cancer(EC)cells in vitro,and to elucidate the related molecular mechanisms in the cell cycle and PI3K/Akt signaling pathway.Methods:EC9706 cells were cultured in RPMI 1640 medium supplemented with 10%calf serum at 37C in a 5%CO2 incubator.The cells were treated with rat serum containing TD or the serum of rats administered Xiaoaiping as a positive control drug.Cell proliferation was assessed by methylthiazolyldiphenyl-tetrazolium bromide assays.Cell morphology was observed under a microscope.The cell cycle was examined by flow cytometry.Protein expression in the PI3K/Akt signaling pathway was measured by western blotting.Results:TD mainly inhibited cell proliferation.Concentrations of 50%cell inhibition by rat serum containing TD or Xiaoaiping were 73.6 and 153.8 mL/mL,respectively.TD also influenced cell morphology characterized by small shrunken cells.Cell colonies became small and the cell proliferation rate was slower.In cell cycle analysis,the percentage of cells in S phase was decreased significantly by TD and Xiaoaiping compared with the blank control group(P<.05).Western blotting showed that serum containing TD strongly downregulated EGFR,PI3K,Akt,p-Akt,and mTOR expression compared with the blank control group(P<.05).Conclusion:TD could inhibit EC9706 carcinoma cell proliferation by blocking the cell cycle progression in S phase.The possible mechanism was inhibition of multiple targets in the PI3K/Akt signaling pathway by TD. 展开更多
关键词 Tonglian decoction Esophageal cancer EC9706 cells Cell cycle PI3K/AKT
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Regulation of Zishen Qinggan( Shuangyi) Prescription to Insulin Resistance of GK Rats
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作者 Chunyu TIAN Chen XING +8 位作者 Haimei BO Liang ZHU Xiaojin LA Huijuan CAO Xin YAN Yuyang YANG Xuemei ZHOU Ji'an LI yongsen jia 《Medicinal Plant》 2017年第3期19-22,共4页
[Objective] To study the effects of Zishen Qinggan( Shuangyi) Prescription on blood glucose,Hb A1c( glycosylated hemoglobin A1c),C-peptide( C-P),glucagon-like peptide( GLP-1),and α-glucosidase activity in GK( Goto-Ka... [Objective] To study the effects of Zishen Qinggan( Shuangyi) Prescription on blood glucose,Hb A1c( glycosylated hemoglobin A1c),C-peptide( C-P),glucagon-like peptide( GLP-1),and α-glucosidase activity in GK( Goto-Kakizaki) rats. [Methods]Selected fasting blood glucose( FBG) > 11. 1mmol/L GK rats and randomly divided into groups: model group,Zishen Qinggan( Shuangyi) Prescription low dosage( ig,400 mg/kg/d),medium dosage( ig,800 mg/kg/d),and high dosage groups( ig,1600 mg/kg/d),and metformin group(ig,85 mg/kg/d). After continuous administration for 28 d,fasting blood glucose(FBG),oral glucose tolerance test(OGTT),Hb A1 c,C-P,GLP-1 and α-glucosidase activity were detected. [Results] Compared with the control group,FBG and Hb A1 c of the model group was significantly higher( P < 0. 01); compared with the model group,Zishen Qinggan( Shuangyi) Prescription could significantly reduce the levels of blood glucose,Hb A1 c,and the elevated blood glucose levels after 120 min of glucose loading in OGTT( P < 0. 05,P < 0. 01),and also can significantly improve the level of C-P,GLP-1( P < 0. 05,P < 0. 01),reduce Homa-IR,and inhibit α-glucosidase activity. [Conclusions]Zishen Qinggan( Shuangyi) Prescription can effectively reduce the blood glucose of GK rats,the action mechanism of which is possibly that it can improve insulin resistance,increase GLP-1 content and inhibit α-glucosidase activity. 展开更多
关键词 Zishen Qinggan(Shuangyi) PRESCRIPTION Type 2 diabetes(diabetes mellitus) INSULIN resistance
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