目的:在既往研究冬连三七组分(Composition of Ophiopogon polysaccharide,Notoginseng total saponins and Rhizoma Coptidis alkaloids,CONR)能改善糖尿病动脉粥样硬化(diabetic atherosclerosis,DA)兔蛋白非酶糖基化基础上,探讨CONR...目的:在既往研究冬连三七组分(Composition of Ophiopogon polysaccharide,Notoginseng total saponins and Rhizoma Coptidis alkaloids,CONR)能改善糖尿病动脉粥样硬化(diabetic atherosclerosis,DA)兔蛋白非酶糖基化基础上,探讨CONR减轻RAS系统激活,提高Na^+-K^+-ATPase活性从而保护DA兔心肌组织的机制。方法:予雄性纯种新西兰大白兔高脂饮食并静脉推注四氧嘧啶且行腹主动脉内膜球囊损伤术诱导DA模型,正常组每日给予生理盐水20 m L灌胃作为对照,实验组分别每日给予辛伐他汀3 mg/kg,CONR 450 mg/kg、150 mg/kg、50 mg/kg;灌胃10周。测定各组大兔心脏重量、左心室重量、心体比、左心室/体重指数、心肌血管紧张素Ⅱ(AngⅡ)、Na^+-K^+-ATPase含量及血管紧张素转化酶(ACE)受体在心肌组织的表达,HE染色法观察大兔心肌病理。结果:与模型组比较,CONR大中剂量组可显著降低DA大兔心脏重量、左心室重量、心体比、左心室/体重指数、心肌组织AngⅡ含量(P<0.05),升高心肌Na^+-K^+-ATPase含量(P<0.01),并抑制心肌ACE受体表达(P<0.01);明显改善了DA兔心肌细胞水肿、炎性细胞浸润、心肌间质纤维排列紊乱增生等病理改变。结论:冬连三七组分可能通过抑制蛋白非酶糖基化,减轻RAS系统激活,提高Na^+-K^+-ATPase活性从而改善DA兔的心肌损伤。展开更多
Objective To inquire into the mechanism of toxic effect of nickel sulfate (NiSO 4) on heart, liver and kidney.Methods Several groups of rats were exposed to NiSO 4 at dose of 2.5,5 0, 10.0 mg/kg through intraperitonea...Objective To inquire into the mechanism of toxic effect of nickel sulfate (NiSO 4) on heart, liver and kidney.Methods Several groups of rats were exposed to NiSO 4 at dose of 2.5,5 0, 10.0 mg/kg through intraperitoneal infection for 10 days, the cell membrane of myocardium, liver and renal tubules were prepared to assess the activity of Na +·K + ATPase, Ca 2+ ATPase with spectrophotometric assay. Results The result showed that NiSO 4 was able to inhibit obviously the activity of Na +·K + ATPase, Ca 2+ ATPase of the three kinds of cell membrane, and its inhibitiue effect was shown to be the strongest in kidney and the weakest in liver.Conclusion The damage on rat’s heart, liver and kidney by NiSO 4 could be related to the inhibitive activity of cell membrane ATPase. However, the mechanism of toxic effect of nickel sulfate on heart, liver and kidney should be studied further.展开更多
文摘目的:在既往研究冬连三七组分(Composition of Ophiopogon polysaccharide,Notoginseng total saponins and Rhizoma Coptidis alkaloids,CONR)能改善糖尿病动脉粥样硬化(diabetic atherosclerosis,DA)兔蛋白非酶糖基化基础上,探讨CONR减轻RAS系统激活,提高Na^+-K^+-ATPase活性从而保护DA兔心肌组织的机制。方法:予雄性纯种新西兰大白兔高脂饮食并静脉推注四氧嘧啶且行腹主动脉内膜球囊损伤术诱导DA模型,正常组每日给予生理盐水20 m L灌胃作为对照,实验组分别每日给予辛伐他汀3 mg/kg,CONR 450 mg/kg、150 mg/kg、50 mg/kg;灌胃10周。测定各组大兔心脏重量、左心室重量、心体比、左心室/体重指数、心肌血管紧张素Ⅱ(AngⅡ)、Na^+-K^+-ATPase含量及血管紧张素转化酶(ACE)受体在心肌组织的表达,HE染色法观察大兔心肌病理。结果:与模型组比较,CONR大中剂量组可显著降低DA大兔心脏重量、左心室重量、心体比、左心室/体重指数、心肌组织AngⅡ含量(P<0.05),升高心肌Na^+-K^+-ATPase含量(P<0.01),并抑制心肌ACE受体表达(P<0.01);明显改善了DA兔心肌细胞水肿、炎性细胞浸润、心肌间质纤维排列紊乱增生等病理改变。结论:冬连三七组分可能通过抑制蛋白非酶糖基化,减轻RAS系统激活,提高Na^+-K^+-ATPase活性从而改善DA兔的心肌损伤。
文摘Objective To inquire into the mechanism of toxic effect of nickel sulfate (NiSO 4) on heart, liver and kidney.Methods Several groups of rats were exposed to NiSO 4 at dose of 2.5,5 0, 10.0 mg/kg through intraperitoneal infection for 10 days, the cell membrane of myocardium, liver and renal tubules were prepared to assess the activity of Na +·K + ATPase, Ca 2+ ATPase with spectrophotometric assay. Results The result showed that NiSO 4 was able to inhibit obviously the activity of Na +·K + ATPase, Ca 2+ ATPase of the three kinds of cell membrane, and its inhibitiue effect was shown to be the strongest in kidney and the weakest in liver.Conclusion The damage on rat’s heart, liver and kidney by NiSO 4 could be related to the inhibitive activity of cell membrane ATPase. However, the mechanism of toxic effect of nickel sulfate on heart, liver and kidney should be studied further.
