The microglia-mediated inflammatory reaction promotes neuronal damage under cerebral isch- emia/hypoxia conditions. We therefore speculated that inhibition of hypoxia-induced microglial activation may alleviate neuron...The microglia-mediated inflammatory reaction promotes neuronal damage under cerebral isch- emia/hypoxia conditions. We therefore speculated that inhibition of hypoxia-induced microglial activation may alleviate neuronal damage. To test this hypothesis, we co-cultured ginsenoside Rb 1, an active component of ginseng, and cortical neurons. Ginsenoside Rb l protected neuronal morphology and structure in a single hypoxic culture system and in a hypoxic co-culture system with microglia, and reduced neuronal apoptosis and caspase-3 production. The protective effect was observable prior to placing in co-culture. Additionally, ginsenoside Rbl inhibited levels of tumor necrosis factor-a in a co-culture system containing activated N9 microglial cells. Ginse-noside Rbl also significantly decreased nitric oxide and superoxide production induced by N9 microglia. Our findings indicate that ginsenoside Rbl attenuates damage to cerebral cortex neu-rons by downregulation of nitric oxide, superoxide, and tumor necrosis factor-a expression in hypoxia-activated microglia.展开更多
目的:本实验通过观察炙甘草汤对缺血缺氧心肌电生理活动的影响,探讨其对心肌的保护和抗心律失常作用的机制。方法:玻璃微电极细胞内记录的方法,观察正常灌流液、缺血缺氧灌流液和缺血缺氧+炙甘草汤(20mg/ml、40mg/ml and 80mg/ml)灌流...目的:本实验通过观察炙甘草汤对缺血缺氧心肌电生理活动的影响,探讨其对心肌的保护和抗心律失常作用的机制。方法:玻璃微电极细胞内记录的方法,观察正常灌流液、缺血缺氧灌流液和缺血缺氧+炙甘草汤(20mg/ml、40mg/ml and 80mg/ml)灌流液对豚鼠左心室流出道慢反应自律细胞及心室乳头肌细胞动作电位的影响。结果:(1)缺血缺氧时左室流出道细胞APD50、APD90和APD均明显缩短(P<0.05),VDD及RPF显著变慢(P<0.01);而加入不同剂量炙甘草汤(20mg/ml、40mg/ml and80mg/ml)可剂量依赖性的拮抗由缺血缺氧介导的APD50、APD90和APD的缩短(P<0.05,0.01或0.001),使VDD及RPF加快基本恢复正常的节律。此种干预作用以80mg/ml炙甘草汤最为明显。(2)缺血缺氧时心室肌细胞的Vmax、APD50和APD90及APD均明显减小(P<0.05);在缺血缺氧灌流液中加入不同剂量的炙甘草汤后上述效应得到明显改善。结论:提示炙甘草汤对缺血缺氧导致的左心室流出道慢反应自律细胞的异常电生理所诱发的心律失常及心肌细胞损伤有显著保护作用。展开更多
基金the National Natural Science Foundation of China,No.81041054China Postdoctoral Science Foundation funded project(General Program),No.2013M542193
文摘The microglia-mediated inflammatory reaction promotes neuronal damage under cerebral isch- emia/hypoxia conditions. We therefore speculated that inhibition of hypoxia-induced microglial activation may alleviate neuronal damage. To test this hypothesis, we co-cultured ginsenoside Rb 1, an active component of ginseng, and cortical neurons. Ginsenoside Rb l protected neuronal morphology and structure in a single hypoxic culture system and in a hypoxic co-culture system with microglia, and reduced neuronal apoptosis and caspase-3 production. The protective effect was observable prior to placing in co-culture. Additionally, ginsenoside Rbl inhibited levels of tumor necrosis factor-a in a co-culture system containing activated N9 microglial cells. Ginse-noside Rbl also significantly decreased nitric oxide and superoxide production induced by N9 microglia. Our findings indicate that ginsenoside Rbl attenuates damage to cerebral cortex neu-rons by downregulation of nitric oxide, superoxide, and tumor necrosis factor-a expression in hypoxia-activated microglia.
文摘目的:本实验通过观察炙甘草汤对缺血缺氧心肌电生理活动的影响,探讨其对心肌的保护和抗心律失常作用的机制。方法:玻璃微电极细胞内记录的方法,观察正常灌流液、缺血缺氧灌流液和缺血缺氧+炙甘草汤(20mg/ml、40mg/ml and 80mg/ml)灌流液对豚鼠左心室流出道慢反应自律细胞及心室乳头肌细胞动作电位的影响。结果:(1)缺血缺氧时左室流出道细胞APD50、APD90和APD均明显缩短(P<0.05),VDD及RPF显著变慢(P<0.01);而加入不同剂量炙甘草汤(20mg/ml、40mg/ml and80mg/ml)可剂量依赖性的拮抗由缺血缺氧介导的APD50、APD90和APD的缩短(P<0.05,0.01或0.001),使VDD及RPF加快基本恢复正常的节律。此种干预作用以80mg/ml炙甘草汤最为明显。(2)缺血缺氧时心室肌细胞的Vmax、APD50和APD90及APD均明显减小(P<0.05);在缺血缺氧灌流液中加入不同剂量的炙甘草汤后上述效应得到明显改善。结论:提示炙甘草汤对缺血缺氧导致的左心室流出道慢反应自律细胞的异常电生理所诱发的心律失常及心肌细胞损伤有显著保护作用。
