目的:染料木黄酮(Genistein)与17β-雌二醇(E2)结构相似,低剂量Genistein可触发雌激素β受体的活性而表现出雌激素样作用,减轻淀粉样β蛋白诱导的神经元退行性变,因而被认为可能是雌激素治疗或预防神经退行性疾病的有效措施。但高剂量Genistein却产生神经毒作用,导致细胞凋亡。目前,有关不同浓度Genistein对痴呆模型大鼠工作记忆影响的比较及其可能机制还未见报道。本实验在侧脑室注射Aβ1-42制备阿尔茨海默病(AD)模型大鼠的基础上,观察了不同剂量的Genistein对AD模型大鼠工作记忆的影响,并探讨了可能的分子机制。方法:将SD大鼠随机分为对照组、Aβ1-42模型组和不同剂量Genistein治疗组。经Y迷宫试验测定各组大鼠空间工作记忆,利用RT-PCR分析大鼠海马组织中STAT3和Caspase-3m RNA相对表达量。结果:(1)与对照组相比,单独给予Aβ1-42的大鼠在Y迷宫试验中自发交替反应率明显降低,海马STAT3的m RNA相对表达量明显降低,但Caspase-3 m RNA相对表达量显著上升;(2)与Aβ1-42组比较,联合给药组中低剂量Genistein(2mg/kg)组大鼠行为学实验自发交替反应率和海马STAT3的m RNA相对表达量明显升高,Caspase-3 m RNA相对表达量则明显降低;给予高剂量Genistein(20mg/kg)后,行为学和PCR检测结果与Aβ1-42组无统计学差异。结论:(1)Aβ1-42可通过上调Caspase-3并抑制STAT3基因表达损伤大鼠工作记忆;(2)低剂量Genistein通过上调STAT3 m RNA同时抑制Caspase-3基因表达拮抗了Aβ1-42诱导的神经毒作用。以上提示,给予低剂量Genistein可能有助于预防或延缓AD患者认知功能的衰退。
It has been documented that the determinants of cardiac excitability are the voltage-gated sodium channel current(INa)and inward rectifier potassium channel current(IK1).However,it is unclear what molecular contributi...
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It has been documented that the determinants of cardiac excitability are the voltage-gated sodium channel current(INa)and inward rectifier potassium channel current(IK1).However,it is unclear what molecular contribution is for the distinct biophysical properties of INa in atrial and ventricular myocytes and the different excitability in cardiac atrium and *** we will discuss our recent novel findings how Navβ2 and Navβ4 contribute to differential biophysical kinetics of INa and pharmacological response to INa blockers in atrial and ventricular myocytes,and the molecular difference related to distinct excitability(higher excitability in atrial than in myocytes),*** distribution of Kir2.3 and Kir2.1 in these myocytes.
Objectives:Angiotensin Ⅱ(AngⅡ),as local hormone in gastrointestinal tract,plays an important role in regulation of smooth muscle motility and smooth muscle ***,it is not clear whether Ang Ⅱ is involved in diabetics...
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Objectives:Angiotensin Ⅱ(AngⅡ),as local hormone in gastrointestinal tract,plays an important role in regulation of smooth muscle motility and smooth muscle ***,it is not clear whether Ang Ⅱ is involved in diabetics-induced loss of gastric *** present study was designed to investigatethe relationship between diabetics-induced loss of gastric ICC and Ang Ⅱ signaling pathway in
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