目的 观察针刺对血管性痴呆(vascular dementia,Va D)大鼠学习记忆能力及半胱天冬酶(cysteinyl aspartate specific proteinase,Caspase)-3通路相关蛋白的影响及其机制研究,探索针刺防治Va D的新靶点。方法 健康雄性SD大鼠随机分为假手...目的 观察针刺对血管性痴呆(vascular dementia,Va D)大鼠学习记忆能力及半胱天冬酶(cysteinyl aspartate specific proteinase,Caspase)-3通路相关蛋白的影响及其机制研究,探索针刺防治Va D的新靶点。方法 健康雄性SD大鼠随机分为假手术组、模型组和针刺组,模型组和针刺组大鼠制备Va D模型,针刺组选取百会和双侧肾俞、丰隆进行针刺干预2周,假手术组和模型组不予其他干预。观察各组大鼠的行为学、海马CA1区形态学改变,检测B淋巴细胞瘤-2基因(B-cell lymphoma-2,Bcl-2)、Caspase-3、Bcl-2相关X蛋白(Bcl-2-associated X protein,Bax) m RNA及蛋白的表达。结果 与假手术组比较,模型组大鼠逃避潜伏期明显延长(P<0.01),穿越平台次数显著减少(P<0.01),大鼠海马组织内Bax、Caspase-3 m RNA及蛋白的表达明显增加(P<0.01),Bcl-2 m RNA及蛋白的表达明显下降(P<0.01)。与模型组比较,针刺组大鼠逃避潜伏期明显缩短(P<0.01),穿越平台次数明显增加(P<0.01),大鼠海马区Bax、Caspase-3 m RNA及蛋白表达明显下降(P<0.01),Bcl-2 m RNA及蛋白水平明显增加(P<0.01)。结论 针刺能提高Va D大鼠的学习记忆能力,其机制可能与调节Caspase-3通路相关蛋白表达、抑制神经元凋亡相关。展开更多
Background:Paclitaxel is a compound derived from Pacific yew bark that induces various cancer cell apoptosis.However,whether it also has anticancer activities in KOSC3 cells,an oral cancer cell line,is unclear.Methods:...Background:Paclitaxel is a compound derived from Pacific yew bark that induces various cancer cell apoptosis.However,whether it also has anticancer activities in KOSC3 cells,an oral cancer cell line,is unclear.Methods:3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide,flow cytometry,and western blotting assays were carried out to assess cell viability,subG1 phase of the cell cycle,and apoptosis-related protein expression,respectively.Results:Ourfindings indicate that paclitaxel could inhibit cell viability and increase the expression of apoptotic markers,including plasma membrane blebbing and the cleavage of poly ADP-ribose polymerase in KOSC3 cells.Also,the treatment with paclitaxel remarkably elevated the percentage of the subG1 phase in KOSC3 cells.In addition,treatment with a pan-caspase inhibitor could recover paclitaxel-inhibited cell viability.Moreover,caspase-8,caspase-9,caspase-7,and BH3 interacting domain death agonist(Bid)were activated in paclitaxel-treated KOSC3 cells.Conclusions:Paclitaxel induced apoptosis through caspase cascade in KOSC3 cells.展开更多
文摘目的 观察针刺对血管性痴呆(vascular dementia,Va D)大鼠学习记忆能力及半胱天冬酶(cysteinyl aspartate specific proteinase,Caspase)-3通路相关蛋白的影响及其机制研究,探索针刺防治Va D的新靶点。方法 健康雄性SD大鼠随机分为假手术组、模型组和针刺组,模型组和针刺组大鼠制备Va D模型,针刺组选取百会和双侧肾俞、丰隆进行针刺干预2周,假手术组和模型组不予其他干预。观察各组大鼠的行为学、海马CA1区形态学改变,检测B淋巴细胞瘤-2基因(B-cell lymphoma-2,Bcl-2)、Caspase-3、Bcl-2相关X蛋白(Bcl-2-associated X protein,Bax) m RNA及蛋白的表达。结果 与假手术组比较,模型组大鼠逃避潜伏期明显延长(P<0.01),穿越平台次数显著减少(P<0.01),大鼠海马组织内Bax、Caspase-3 m RNA及蛋白的表达明显增加(P<0.01),Bcl-2 m RNA及蛋白的表达明显下降(P<0.01)。与模型组比较,针刺组大鼠逃避潜伏期明显缩短(P<0.01),穿越平台次数明显增加(P<0.01),大鼠海马区Bax、Caspase-3 m RNA及蛋白表达明显下降(P<0.01),Bcl-2 m RNA及蛋白水平明显增加(P<0.01)。结论 针刺能提高Va D大鼠的学习记忆能力,其机制可能与调节Caspase-3通路相关蛋白表达、抑制神经元凋亡相关。
基金The present study was supported by the National Science and Technology Council,Taiwan(MOST-107-2320-B-471-001 to YYL and MOST-110-2320-B-006-025-MY3 to BMH)by An Nan Hospital(ANHRF111-55 to TCC and BMH).
文摘Background:Paclitaxel is a compound derived from Pacific yew bark that induces various cancer cell apoptosis.However,whether it also has anticancer activities in KOSC3 cells,an oral cancer cell line,is unclear.Methods:3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide,flow cytometry,and western blotting assays were carried out to assess cell viability,subG1 phase of the cell cycle,and apoptosis-related protein expression,respectively.Results:Ourfindings indicate that paclitaxel could inhibit cell viability and increase the expression of apoptotic markers,including plasma membrane blebbing and the cleavage of poly ADP-ribose polymerase in KOSC3 cells.Also,the treatment with paclitaxel remarkably elevated the percentage of the subG1 phase in KOSC3 cells.In addition,treatment with a pan-caspase inhibitor could recover paclitaxel-inhibited cell viability.Moreover,caspase-8,caspase-9,caspase-7,and BH3 interacting domain death agonist(Bid)were activated in paclitaxel-treated KOSC3 cells.Conclusions:Paclitaxel induced apoptosis through caspase cascade in KOSC3 cells.
