目的:观察HCN1,HCN2在功能性便秘(function constipation,FC)大鼠模型结肠上的表达及其与结肠Cajal间质细胞(interstitial cells of Cajal,ICCs)细胞之间的关系,探讨HCN1,HCN2对FC发病的影响。方法:用复方地芬诺酯制造FC大鼠模型,利用...目的:观察HCN1,HCN2在功能性便秘(function constipation,FC)大鼠模型结肠上的表达及其与结肠Cajal间质细胞(interstitial cells of Cajal,ICCs)细胞之间的关系,探讨HCN1,HCN2对FC发病的影响。方法:用复方地芬诺酯制造FC大鼠模型,利用免疫组织化学分别对模型组(n=12)、空白组(n=12)大鼠升结肠、横结肠、降结肠黏膜HCN1,HCN2及ICC的表达情况进行检测。结果:模型组和空白组升结肠、横结肠及降结肠均见HCN1,HCN2,c-Kit表达,模型组中HCN1,HCN2,c-Kit表达量明显低于空白组(P<0.05);HCN1表达在FC大鼠结肠中主要分布在结肠环形肌和纵行肌之间的肌ICC-MY,与c-Kit表达分布基本一致;HCN2在FC大鼠升结肠、横结肠及降结肠均有分布与c-Kit荧光度变化趋势基本一致。HCN2阳性神经元与ICCs的突起距离较近,二者未见细胞共存现象。结论:HCN通道作为一种与自主起博活动密切相关的离子通道,可能参与结肠ICCs的自主起博活动。HCN1,HCN2可能参与结肠运动调控,其数量、功能及分布异常可能与FC发病机制有关。展开更多
目的通过风湿性心脏病(简称风心病)心房颤动(简称房颤)患者右心耳组织超极化激活环核苷酸门控阳离子通道-2(HCN2)基因mRNA表达检测,探讨其与房颤的可能关系。方法 28例风心病患者根据是否存在房颤,分为房颤组和窦性心律(简称窦律)组,术...目的通过风湿性心脏病(简称风心病)心房颤动(简称房颤)患者右心耳组织超极化激活环核苷酸门控阳离子通道-2(HCN2)基因mRNA表达检测,探讨其与房颤的可能关系。方法 28例风心病患者根据是否存在房颤,分为房颤组和窦性心律(简称窦律)组,术前均行心脏彩色多普勒超声检测,术中取右心耳组织,应用半定量聚合酶链式反应技术检测HCN2mRNA表达。结果房颤组右房径大于窦律组((59.2±10.9 mm vs 41.7±15.5mm,P<0.05);HCN2mRNA表达水平高于窦律组(0.911 9±0.7052 vs 0.4735±0.3909,P<0.05)。结论HCN2mRNA表达异常增高,可能与风心病房颤的发生相关。展开更多
Aim To investigate whether tluoxetine, a selective serotonin reuptake inhibitor（ SSRI） , could amelio- rate cognitive impairments induced by chronic cerebral hypopeffusion in rats and to clarify the underlying mecha...Aim To investigate whether tluoxetine, a selective serotonin reuptake inhibitor（ SSRI） , could amelio- rate cognitive impairments induced by chronic cerebral hypopeffusion in rats and to clarify the underlying mecha- nisms of its efficacy. Methods Rats were subjected to permanent bilateral occlusion of the common carotid arteries （two-vessel occlusion, 2VO）. Two weeks later, rats were treated with 30 mg · kg^-1 fluoxetine （intragastric injec- tion, i. g. ） for 6 weeks. Cognitive function was evaluated by Morris water maze （MWM） and novel objects recog- nition （NOR） test. Long-term potentiation （LTP） was used to address the underlying synaptic mechanisms. West- ern blot was used to quantify the protein levels. Results Fluoxetine treatment significantly improved the cognitive 2VO impairments caused by 2VO, accompanied with a reversion of 2VO-induced inhibitory of LTP. Furthermore, caused an up-regulation of hyperpolarization-activated cyclic nueleotide-gated channel 2 （HCN2） surface expres- sions in the hippocampal CA1 area and fluoxetine also effectively recovered the up-regulation of HCN2 surface ex- pressions. Conclusion Fluoxetine can ameliorate cognitive impairments induced by chronic cerebral hypopeffusion and a possible mechanism may via down-regulating HCN2 surface expression in the Hippocampal CA1 area.展开更多
文摘目的:观察HCN1,HCN2在功能性便秘(function constipation,FC)大鼠模型结肠上的表达及其与结肠Cajal间质细胞(interstitial cells of Cajal,ICCs)细胞之间的关系,探讨HCN1,HCN2对FC发病的影响。方法:用复方地芬诺酯制造FC大鼠模型,利用免疫组织化学分别对模型组(n=12)、空白组(n=12)大鼠升结肠、横结肠、降结肠黏膜HCN1,HCN2及ICC的表达情况进行检测。结果:模型组和空白组升结肠、横结肠及降结肠均见HCN1,HCN2,c-Kit表达,模型组中HCN1,HCN2,c-Kit表达量明显低于空白组(P<0.05);HCN1表达在FC大鼠结肠中主要分布在结肠环形肌和纵行肌之间的肌ICC-MY,与c-Kit表达分布基本一致;HCN2在FC大鼠升结肠、横结肠及降结肠均有分布与c-Kit荧光度变化趋势基本一致。HCN2阳性神经元与ICCs的突起距离较近,二者未见细胞共存现象。结论:HCN通道作为一种与自主起博活动密切相关的离子通道,可能参与结肠ICCs的自主起博活动。HCN1,HCN2可能参与结肠运动调控,其数量、功能及分布异常可能与FC发病机制有关。
文摘目的通过风湿性心脏病(简称风心病)心房颤动(简称房颤)患者右心耳组织超极化激活环核苷酸门控阳离子通道-2(HCN2)基因mRNA表达检测,探讨其与房颤的可能关系。方法 28例风心病患者根据是否存在房颤,分为房颤组和窦性心律(简称窦律)组,术前均行心脏彩色多普勒超声检测,术中取右心耳组织,应用半定量聚合酶链式反应技术检测HCN2mRNA表达。结果房颤组右房径大于窦律组((59.2±10.9 mm vs 41.7±15.5mm,P<0.05);HCN2mRNA表达水平高于窦律组(0.911 9±0.7052 vs 0.4735±0.3909,P<0.05)。结论HCN2mRNA表达异常增高,可能与风心病房颤的发生相关。
文摘Aim To investigate whether tluoxetine, a selective serotonin reuptake inhibitor（ SSRI） , could amelio- rate cognitive impairments induced by chronic cerebral hypopeffusion in rats and to clarify the underlying mecha- nisms of its efficacy. Methods Rats were subjected to permanent bilateral occlusion of the common carotid arteries （two-vessel occlusion, 2VO）. Two weeks later, rats were treated with 30 mg · kg^-1 fluoxetine （intragastric injec- tion, i. g. ） for 6 weeks. Cognitive function was evaluated by Morris water maze （MWM） and novel objects recog- nition （NOR） test. Long-term potentiation （LTP） was used to address the underlying synaptic mechanisms. West- ern blot was used to quantify the protein levels. Results Fluoxetine treatment significantly improved the cognitive 2VO impairments caused by 2VO, accompanied with a reversion of 2VO-induced inhibitory of LTP. Furthermore, caused an up-regulation of hyperpolarization-activated cyclic nueleotide-gated channel 2 （HCN2） surface expres- sions in the hippocampal CA1 area and fluoxetine also effectively recovered the up-regulation of HCN2 surface ex- pressions. Conclusion Fluoxetine can ameliorate cognitive impairments induced by chronic cerebral hypopeffusion and a possible mechanism may via down-regulating HCN2 surface expression in the Hippocampal CA1 area.
