目的研究糖尿病高胆固醇血症患者应用匹伐他汀治疗的临床效果。方法回顾性分析2012年5月至2014年5月内分泌科治疗的87例糖尿病高胆固醇血症患者临床资料,依据治疗方式将其分为研究组44例与对照组43例,均予糖尿病、低脂饮食,配合运动指导及降糖药物口服或胰岛素皮下注射,研究组予匹伐他汀口服治疗,对照组予阿托伐他汀口服治疗,两组均连续治疗6周。结果研究组总有效率为97.73%,优于对照组的88.37%(P<0.05)。研究组治疗后空腹血糖(FBG)、餐后2 h血糖(2 h PG)、糖化血红蛋白(Hb A1C)、总胆固醇(TC)、三酰甘油(TG)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)水平与对照组相比,差异明显(P<0.05)。研究组不良反应发生率为4.55%,低于对照组的16.28%(P<0.05)。结论糖尿病高胆固醇血症应用匹伐他汀治疗,不仅能改善患者血糖水平,且可纠正血脂代谢紊乱,不良反应少,效果显著,值得推广。
目的:研究富氢水对糖尿病小鼠肾脏的保护作用,并探讨其可能的作用机制。方法:60只健康ICR雄性小鼠,随机分成空白对照组(A组)、糖尿病组(B组)和糖尿病富氢水干预组(C组)。链脲佐菌素(STZ)150 mg/kg腹腔注射诱发糖尿病,造模成功后,C组每日腹腔注射富氢水5 m L/kg,B组腹腔注射等量0.9%氯化钠溶液,连续8周。尾静脉取血测定小鼠血糖,HE染色观察肾脏组织学变化,免疫组织化学染色观察NADPH氧化酶4(Nox4)和血红素加氧酶-1(HO-1)蛋白的表达。结果:C组Nox4表达水平明显低于B组,而HO-1表达明显高于B组;B组与C组的空腹血糖均明显高于A组(P<0.01),B组与C组之间差异无统计学意义(P>0.05);3组肾脏组织病理HE染色未显示明显病变。结论:富氢水可减轻糖尿病小鼠肾脏组织的氧化应激水平。
Endothelium lines vascular walls and regulates vascular *** endothelial cells sense and respond to chemical and mechanical stimuli in the circulation,and couple the stimulus signals to vascular smooth muscles,in which...
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Endothelium lines vascular walls and regulates vascular *** endothelial cells sense and respond to chemical and mechanical stimuli in the circulation,and couple the stimulus signals to vascular smooth muscles,in which several membrane receptors and ion channels play a *** about these surface-expressing proteins may help to understand endothelium function and its role in certain vascular *** we show a K+current in primarily cultured pulmonary arterial endothelial cells(PAECs)that is regulated by the Ca2+/calmodulin(Ca M)-dependent protein kinase Ⅱ(Ca MKⅡ).In whole-cell voltage clamp,the PAECs showed large inward rectifier K+currents that were sensitive to micromolar concentrations of extracellular Ba2+,but insensitive to intracellular ATP and p *** excised inside-out patches,an inward rectifier K+current was observed with single-channel conductance 32.43±0.45 p S and Popen 0.27±*** PCR analysis showed strong expression of Kir2.1 in the endothelial *** current did not respond to intracellular GDP-β-S and extracellular cholera *** vascular regulators were *** K+current was insensitive to carbachol,neither to the e NOS inhibitor *** to the Ca M inhibitor W-7 and Ca MKⅡ inhibitor KN-62 strongly suppressed the ***,vasodilation was suppressed by W-7 and Ba2+in isolated and perfused pulmonary arterial ***,these results suggest that the PAECs express an inward rectifier K+current that is likely to be Kir2.1,and such a K+channel appears to be targeted by Ca MKⅡ-dependent intracellular signaling systems.
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