The glucose isomerase(GI) was a metal activating enzyme It was most activated by Co 2+ and Mg 2+ ,and Mg 2+ was the best activator,whether the glucose or the xylose was the substrate When the glucose was substrate,the...The glucose isomerase(GI) was a metal activating enzyme It was most activated by Co 2+ and Mg 2+ ,and Mg 2+ was the best activator,whether the glucose or the xylose was the substrate When the glucose was substrate,the dissociation constant of Mg 2+ GI,Co 2+ GI and Mn 2+ -GI was 115 μmol/L,40 μmol/L, and 15 μmol/L respectively. The maximum activity of Mg 2+ GI,Co 2- GI and Mn 2+ GI was 100%,85%,and 20% respectively. When the xylose was substrate,the order of dissociation constant and maximum activity of the metal enzymes was the same Ca 2+ was a competitive inhibitor versus Mg 2+ ( K i 7 4 μmol/L)or Co 2+ ( K i 99 μmol/L). Compared with Mg 2+ GI,the K m of Co 2+ GI was more,and the V M of Co 2+ GI less The process of activity recovery from apo GI to metal GI showed that it was slow and of two展开更多
目的:研究扩心方对阿霉素诱导扩张型心肌病模型大鼠心功能、心肌损伤的保护作用,探讨扩心方作用机制。方法:50只Wistar大鼠腹腔注射阿霉素6周建立DCM模型,开始造模4周后随机分为模型组,扩心方高、中、低剂量组,卡托普利组(每组各10只),...目的:研究扩心方对阿霉素诱导扩张型心肌病模型大鼠心功能、心肌损伤的保护作用,探讨扩心方作用机制。方法:50只Wistar大鼠腹腔注射阿霉素6周建立DCM模型,开始造模4周后随机分为模型组,扩心方高、中、低剂量组,卡托普利组(每组各10只),连续灌胃给药四周,另设10只正常对照。正常组和模型组以生理盐水灌胃。治疗结束后,对各组大鼠进行心脏超声检查,病理形态学检测,以及用反转录-聚合酶链反应和蛋白质免疫印迹法分别检测心肌组织中SERCA2α、PLB的m RNA和蛋白含量。结果:与正常对照组相比,模型组心功能减弱,出现心肌病理损害,SERCA2α与PLB表达异常;与模型组相比,扩心方组可以改善DCM大鼠的心功能、心肌病理学形态,同时,提高SERCA2αm RNA和蛋白表达、抑制PLB m RNA和蛋白表达。结论:扩心方能提高DCM大鼠的左心室射血分数和缩短率,减轻心肌损伤,改善心功能,同时调控DCM大鼠SERCA2α、PLB的表达。提示扩心方改善DCM大鼠心功能的作用机制,可能与纠正心肌肌浆网钙调控相关蛋白-SERCA2α、PLB的异常表达相关。展开更多
文摘The glucose isomerase(GI) was a metal activating enzyme It was most activated by Co 2+ and Mg 2+ ,and Mg 2+ was the best activator,whether the glucose or the xylose was the substrate When the glucose was substrate,the dissociation constant of Mg 2+ GI,Co 2+ GI and Mn 2+ -GI was 115 μmol/L,40 μmol/L, and 15 μmol/L respectively. The maximum activity of Mg 2+ GI,Co 2- GI and Mn 2+ GI was 100%,85%,and 20% respectively. When the xylose was substrate,the order of dissociation constant and maximum activity of the metal enzymes was the same Ca 2+ was a competitive inhibitor versus Mg 2+ ( K i 7 4 μmol/L)or Co 2+ ( K i 99 μmol/L). Compared with Mg 2+ GI,the K m of Co 2+ GI was more,and the V M of Co 2+ GI less The process of activity recovery from apo GI to metal GI showed that it was slow and of two
文摘目的:研究扩心方对阿霉素诱导扩张型心肌病模型大鼠心功能、心肌损伤的保护作用,探讨扩心方作用机制。方法:50只Wistar大鼠腹腔注射阿霉素6周建立DCM模型,开始造模4周后随机分为模型组,扩心方高、中、低剂量组,卡托普利组(每组各10只),连续灌胃给药四周,另设10只正常对照。正常组和模型组以生理盐水灌胃。治疗结束后,对各组大鼠进行心脏超声检查,病理形态学检测,以及用反转录-聚合酶链反应和蛋白质免疫印迹法分别检测心肌组织中SERCA2α、PLB的m RNA和蛋白含量。结果:与正常对照组相比,模型组心功能减弱,出现心肌病理损害,SERCA2α与PLB表达异常;与模型组相比,扩心方组可以改善DCM大鼠的心功能、心肌病理学形态,同时,提高SERCA2αm RNA和蛋白表达、抑制PLB m RNA和蛋白表达。结论:扩心方能提高DCM大鼠的左心室射血分数和缩短率,减轻心肌损伤,改善心功能,同时调控DCM大鼠SERCA2α、PLB的表达。提示扩心方改善DCM大鼠心功能的作用机制,可能与纠正心肌肌浆网钙调控相关蛋白-SERCA2α、PLB的异常表达相关。
