Objective: To evaluate the effects and possible mechanisms of rutaecarpine on angiotensin Ⅱ (Ang Ⅱ )-induced proliferation in cultured rat vascular smooth muscle cells (VSMCs). Methods: VSMCs were isolated fro...Objective: To evaluate the effects and possible mechanisms of rutaecarpine on angiotensin Ⅱ (Ang Ⅱ )-induced proliferation in cultured rat vascular smooth muscle cells (VSMCs). Methods: VSMCs were isolated from Male Sprague-Dawley rat aorta, and cultured by enzymic dispersion method. Experiments were performed with cells from passages 3-8. The cultured VSMCs were randomly divided into control, model (Ang Ⅱ 0.1 μ moVL), and rutaecarpine (0.3-3.0μmol/L) groups. VMSC proliferation was induced by Ang Ⅱ, and was evaluated by the 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide assay and cell counting. To examine the mechanisms involved in anti-proliferative effects of rutaecarpine, nitric oxide (NO) levels and NO synthetase (NOS) activity were determined. Expressions of VSMC proliferation-related genes including endothelial nitric oxide synthase (eNOS), and c-myc hypertension related gene-1 (HRG-1) were determined by real-time reverse chain reaction (RT-PCR). Results: Rutaecarpine (0.3-3.0μmol/l_) inhibited Ang R-induced VSMC proliferation and the best effects were achieved at 3.0 μmol/L. The Ang Ⅱ-induced decreases in cellular NO contents and NOS activities were antagonized by rutaecarpine (P〈0.05). Ang Ⅱ administration suppressed the expressions of eNOS and HRG-1, while increased c-myc expression (P〈0.05). All these effects were attenuated by 3.0μmol/L rutaecarpine (P〈0.05). Conclusion: Rutaecarpine is effective against Ang Ⅱ-induced rat VSMC proliferation, and this effect is due, at least in part, to NO production and the modulation of VMSC proliferation-related gene expressions.展开更多
Graft-versus-host disease (GVHD) is a severe complication and a major source of morbidity and mortality after allogeneic hematopoietic stem cell transplantation (HSCT). Although T cell depletion of the allogeneic ...Graft-versus-host disease (GVHD) is a severe complication and a major source of morbidity and mortality after allogeneic hematopoietic stem cell transplantation (HSCT). Although T cell depletion of the allogeneic HSCT can efficiently prevent GVHD, it is associated with increased graft rejection and relapse of the malignant disease. To preserve the beneficial effects of donor T cells and avoid their GVHD effects, some approaches have been explored. One of them is to transfer a special suicide gene into the donor T lymphocytes so that they become more sensitive to a specific drug that is ordinarily not toxic. The most commonly used suicide gene is the thymidine kinase-encoding gene of herpes simplex virus (HSV-tk).展开更多
基金Supported by the National Natural Science Foundation of China(No.81160528)the Governor Foundation of Guizhou Province(No.2006-07)Administration of Traditional Chinese Medicine of Guizhou Province Foundation(No.2009-79)
文摘Objective: To evaluate the effects and possible mechanisms of rutaecarpine on angiotensin Ⅱ (Ang Ⅱ )-induced proliferation in cultured rat vascular smooth muscle cells (VSMCs). Methods: VSMCs were isolated from Male Sprague-Dawley rat aorta, and cultured by enzymic dispersion method. Experiments were performed with cells from passages 3-8. The cultured VSMCs were randomly divided into control, model (Ang Ⅱ 0.1 μ moVL), and rutaecarpine (0.3-3.0μmol/L) groups. VMSC proliferation was induced by Ang Ⅱ, and was evaluated by the 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide assay and cell counting. To examine the mechanisms involved in anti-proliferative effects of rutaecarpine, nitric oxide (NO) levels and NO synthetase (NOS) activity were determined. Expressions of VSMC proliferation-related genes including endothelial nitric oxide synthase (eNOS), and c-myc hypertension related gene-1 (HRG-1) were determined by real-time reverse chain reaction (RT-PCR). Results: Rutaecarpine (0.3-3.0μmol/l_) inhibited Ang R-induced VSMC proliferation and the best effects were achieved at 3.0 μmol/L. The Ang Ⅱ-induced decreases in cellular NO contents and NOS activities were antagonized by rutaecarpine (P〈0.05). Ang Ⅱ administration suppressed the expressions of eNOS and HRG-1, while increased c-myc expression (P〈0.05). All these effects were attenuated by 3.0μmol/L rutaecarpine (P〈0.05). Conclusion: Rutaecarpine is effective against Ang Ⅱ-induced rat VSMC proliferation, and this effect is due, at least in part, to NO production and the modulation of VMSC proliferation-related gene expressions.
文摘Graft-versus-host disease (GVHD) is a severe complication and a major source of morbidity and mortality after allogeneic hematopoietic stem cell transplantation (HSCT). Although T cell depletion of the allogeneic HSCT can efficiently prevent GVHD, it is associated with increased graft rejection and relapse of the malignant disease. To preserve the beneficial effects of donor T cells and avoid their GVHD effects, some approaches have been explored. One of them is to transfer a special suicide gene into the donor T lymphocytes so that they become more sensitive to a specific drug that is ordinarily not toxic. The most commonly used suicide gene is the thymidine kinase-encoding gene of herpes simplex virus (HSV-tk).