目的探讨丝裂原活化蛋白激酶(mitogen-activated protein kinases,MAPKs)―细胞外信号调节激酶1和2(extracellular signal regulated kinase1/2,ERK1/2)信号转导通路在复方丹参注射液对人足月妊娠羊膜上皮细胞水通道蛋白3(aquaporin3,AQ...目的探讨丝裂原活化蛋白激酶(mitogen-activated protein kinases,MAPKs)―细胞外信号调节激酶1和2(extracellular signal regulated kinase1/2,ERK1/2)信号转导通路在复方丹参注射液对人足月妊娠羊膜上皮细胞水通道蛋白3(aquaporin3,AQP3)表达调节中的作用。方法原代培养足月妊娠羊水量正常与羊水过少人羊膜上皮细胞,将人羊膜上皮细胞均分为4组:分别为空白对照组、U0126组、复方丹参注射液组和U0126加复方丹参注射液组。采用免疫印迹技术检测人羊膜上皮细胞中磷酸化ERK1/2(p-ERK1/2)和AQP3的表达。结果 (1)在羊水量正常和羊水过少人羊膜上皮细胞中,均发现p-ERK1/2表达水平在U0126组较空白对照组明显下降(P<0.05),而复方丹参注射液组可以明显上调p-ERK1/2表达水平(P<0.05),U0126加复方丹参注射液组人羊膜上皮细胞中p-ERK1/2表达水平高于U0126组,但低于复方丹参注射液组(P<0.05)。(2)在羊水量正常的人羊膜上皮细胞中,U0126组AQP3的表达与空白对照组比较无明显变化(P>0.05);复方丹参注射液组和U0126加复方丹参注射液组AQP3的表达水平均高于空白对照组(P<0.05),但两组间比较差异无统计学意义(P>0.05)。(3)在羊水过少羊膜上皮细胞中,U0126组AQP3的表达较空白对照组下降(P<0.05);复方丹参注射液组可以明显上调AQP3的表达水平(P<0.05),而U0126加复方丹参注射液组AQP3的表达水平低于复方丹参注射液组(P<0.05),但高于U0126组(P<0.05)。结论羊水过少时,复方丹参注射液通过激活MAPK-ERK1/2信号转导通路来调节人羊膜上皮细胞中AQP3的表达水平。展开更多
The present study employed a rat model of T10 spinal cord transection. Western blot analyses revealed increased brain-dedved neurotrophic factor (BDNF) expression in spinal cord segments caudal to the transection si...The present study employed a rat model of T10 spinal cord transection. Western blot analyses revealed increased brain-dedved neurotrophic factor (BDNF) expression in spinal cord segments caudal to the transection site following injection of replication incompetent herpes simplex virus vector (HSV-BDNF) into the subarachnoid space. In addition, hindlimb locomotor functions were improved. In contrast, BDNF levels decreased following treatment with replication defective herpes simplex virus vector construct small interference BDNF (HSV-siBDNF). Moreover, hindlimb locomotor functions gradually worsened. Compared with the replication incompetent herpes simplex virus vector control group, extracellular signal regulated kinasel/2 expression increased in the HSV-BDNF group on days 14 and 28 after spinal cord transection, but expression was reduced in the HSV-siBDNF group. These results suggested that BDNF plays an important role in neural plasticity via extracellular signal regulated kinasel/2 signaling pathway in a rat model of adult spina cord transection.展开更多
文摘目的探讨丝裂原活化蛋白激酶(mitogen-activated protein kinases,MAPKs)―细胞外信号调节激酶1和2(extracellular signal regulated kinase1/2,ERK1/2)信号转导通路在复方丹参注射液对人足月妊娠羊膜上皮细胞水通道蛋白3(aquaporin3,AQP3)表达调节中的作用。方法原代培养足月妊娠羊水量正常与羊水过少人羊膜上皮细胞,将人羊膜上皮细胞均分为4组:分别为空白对照组、U0126组、复方丹参注射液组和U0126加复方丹参注射液组。采用免疫印迹技术检测人羊膜上皮细胞中磷酸化ERK1/2(p-ERK1/2)和AQP3的表达。结果 (1)在羊水量正常和羊水过少人羊膜上皮细胞中,均发现p-ERK1/2表达水平在U0126组较空白对照组明显下降(P<0.05),而复方丹参注射液组可以明显上调p-ERK1/2表达水平(P<0.05),U0126加复方丹参注射液组人羊膜上皮细胞中p-ERK1/2表达水平高于U0126组,但低于复方丹参注射液组(P<0.05)。(2)在羊水量正常的人羊膜上皮细胞中,U0126组AQP3的表达与空白对照组比较无明显变化(P>0.05);复方丹参注射液组和U0126加复方丹参注射液组AQP3的表达水平均高于空白对照组(P<0.05),但两组间比较差异无统计学意义(P>0.05)。(3)在羊水过少羊膜上皮细胞中,U0126组AQP3的表达较空白对照组下降(P<0.05);复方丹参注射液组可以明显上调AQP3的表达水平(P<0.05),而U0126加复方丹参注射液组AQP3的表达水平低于复方丹参注射液组(P<0.05),但高于U0126组(P<0.05)。结论羊水过少时,复方丹参注射液通过激活MAPK-ERK1/2信号转导通路来调节人羊膜上皮细胞中AQP3的表达水平。
文摘The present study employed a rat model of T10 spinal cord transection. Western blot analyses revealed increased brain-dedved neurotrophic factor (BDNF) expression in spinal cord segments caudal to the transection site following injection of replication incompetent herpes simplex virus vector (HSV-BDNF) into the subarachnoid space. In addition, hindlimb locomotor functions were improved. In contrast, BDNF levels decreased following treatment with replication defective herpes simplex virus vector construct small interference BDNF (HSV-siBDNF). Moreover, hindlimb locomotor functions gradually worsened. Compared with the replication incompetent herpes simplex virus vector control group, extracellular signal regulated kinasel/2 expression increased in the HSV-BDNF group on days 14 and 28 after spinal cord transection, but expression was reduced in the HSV-siBDNF group. These results suggested that BDNF plays an important role in neural plasticity via extracellular signal regulated kinasel/2 signaling pathway in a rat model of adult spina cord transection.