Ginsenoside Rb1 has been reported to exert anti-aging and anti-neurodegenerative effects. In the present study, we investigate whether ginsenoside Rb1 is involved in neurite outgrowth and neuroprotection against damag...Ginsenoside Rb1 has been reported to exert anti-aging and anti-neurodegenerative effects. In the present study, we investigate whether ginsenoside Rb1 is involved in neurite outgrowth and neuroprotection against damage induced by amyloid beta（25–35） in cultured hippocampal neurons, and explore the underlying mechanisms. Ginsenoside Rb1 significantly increased neurite outgrowth in hippocampal neurons, and increased the expression of phosphorylated-Akt and phosphorylated extracellular signal-regulated kinase 1/2. These effects were abrogated by API-2 and PD98059, inhibitors of the signaling proteins Akt and MEK. Additionally, cultured hippocampal neurons were exposed to amyloid beta（25–35） for 30 minutes; ginsenoside Rb1 prevented apoptosis induced by amyloid beta（25–35）, and this effect was blocked by API-2 and PD98059. Furthermore, ginsenoside Rb1 significantly reversed the reduction in phosphorylated-Akt and phosphorylated extracellular signal-regulated kinase 1/2 levels induced by amyloid beta（25–35）, and API-2 neutralized the effect of ginsenoside Rb1. The present results indicate that ginsenoside Rb1 enhances neurite outgrowth and protects against neurotoxicity induced by amyloid beta（25–35） via a mechanism involving Akt and extracellular signal-regulated kinase 1/2 signaling.展开更多
Despite advances in screening and treatment,colon cancer remains one of the leading causes of cancer-related death.Finding novel and useful drug treatment targets is also an urgent need for clinical applications.Tetra...Despite advances in screening and treatment,colon cancer remains one of the leading causes of cancer-related death.Finding novel and useful drug treatment targets is also an urgent need for clinical applications.Tetrandrine(Tet)is extracted from the Chinese medicinal herbal medicine,which is a well-known calcium blocker with a variety of pharmacological activities,including anti-cancer.In this study,we recruited cell viability assay,flow cytometry analysis,cloning formation to confirm that Tet can inhibit the proliferation of SW620 cells,and induce apoptosis.Mechanically,we confirmed that Tet up-regulates the mRNA and protein level of BMP9 in SW620 cells.Over-expression BMP9 enhances the anticancer effects of Tet in SW620 cells,but these effects can be partly reversed by silencing BMP9.Also,Tet reduces phosphorylation of Aktl/2/3 in SW620 cells,which could be elevated by overexpressed BMP9 and impaired by silencing BMP9.Furthermore,we demonstrated that Tet reduces phosphorylated PTEN,which can be promoted by overexpressed BMP9,analogously also be attenuated through silencing BMP9.Finally,we introduced a xenograft tumor model to investigate the anti-proliferative effect of Tet,further to explore the effects of BMP9 and PTEN in SW620 cells.Our findings suggested that the anti-cancer activity of Tet in SW620 cells may be mediated partly by up-regulating BMP9,followed by inactivation PI3K/Akt through up-regulating PTEN at least.展开更多
基金supported by grants from the National Natural Science Foundation of China,No.30971531,81070987
文摘Ginsenoside Rb1 has been reported to exert anti-aging and anti-neurodegenerative effects. In the present study, we investigate whether ginsenoside Rb1 is involved in neurite outgrowth and neuroprotection against damage induced by amyloid beta（25–35） in cultured hippocampal neurons, and explore the underlying mechanisms. Ginsenoside Rb1 significantly increased neurite outgrowth in hippocampal neurons, and increased the expression of phosphorylated-Akt and phosphorylated extracellular signal-regulated kinase 1/2. These effects were abrogated by API-2 and PD98059, inhibitors of the signaling proteins Akt and MEK. Additionally, cultured hippocampal neurons were exposed to amyloid beta（25–35） for 30 minutes; ginsenoside Rb1 prevented apoptosis induced by amyloid beta（25–35）, and this effect was blocked by API-2 and PD98059. Furthermore, ginsenoside Rb1 significantly reversed the reduction in phosphorylated-Akt and phosphorylated extracellular signal-regulated kinase 1/2 levels induced by amyloid beta（25–35）, and API-2 neutralized the effect of ginsenoside Rb1. The present results indicate that ginsenoside Rb1 enhances neurite outgrowth and protects against neurotoxicity induced by amyloid beta（25–35） via a mechanism involving Akt and extracellular signal-regulated kinase 1/2 signaling.
基金We thank Professor T.C.He(Medical Center of University of Chicago,Chicago IL,USA)for his kind provision of the recombinant adenoviruses.
文摘Despite advances in screening and treatment,colon cancer remains one of the leading causes of cancer-related death.Finding novel and useful drug treatment targets is also an urgent need for clinical applications.Tetrandrine(Tet)is extracted from the Chinese medicinal herbal medicine,which is a well-known calcium blocker with a variety of pharmacological activities,including anti-cancer.In this study,we recruited cell viability assay,flow cytometry analysis,cloning formation to confirm that Tet can inhibit the proliferation of SW620 cells,and induce apoptosis.Mechanically,we confirmed that Tet up-regulates the mRNA and protein level of BMP9 in SW620 cells.Over-expression BMP9 enhances the anticancer effects of Tet in SW620 cells,but these effects can be partly reversed by silencing BMP9.Also,Tet reduces phosphorylation of Aktl/2/3 in SW620 cells,which could be elevated by overexpressed BMP9 and impaired by silencing BMP9.Furthermore,we demonstrated that Tet reduces phosphorylated PTEN,which can be promoted by overexpressed BMP9,analogously also be attenuated through silencing BMP9.Finally,we introduced a xenograft tumor model to investigate the anti-proliferative effect of Tet,further to explore the effects of BMP9 and PTEN in SW620 cells.Our findings suggested that the anti-cancer activity of Tet in SW620 cells may be mediated partly by up-regulating BMP9,followed by inactivation PI3K/Akt through up-regulating PTEN at least.
