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目的观察补阳还五汤对血管性痴呆(VD)大鼠学习记忆能力和海马神经元形态的影响。方法将60只大鼠随机分为5组:正常对照组、假手术组、模型组、补阳还五汤组、尼莫地平组。补阳还五汤组药量为50g/(kg·d),尼莫地平组药量为20mg/(kg·d),共给药30d。模型组、假手术组和正常对照组均给予蒸馏水1mL/100g灌胃。治疗后以Morris水迷宫检测其学习记忆行为能力,以HE染色、Nissl染色检测其神经细胞形态学的变化。结果Morris水迷宫实验中,正常对照组、假手术组、模型组、补阳还五汤组、尼莫地平组的逃避潜伏期分别为:7.67s±3.42s、8.76s±4.03s、29.56s±13.28s、16.96s±7.06s、20.16s±8.89s;探索次数分别为:16.86/min±5.37/min、14.42/min±4.01/min、4.26/min±0.80/min、8.96/min±1.30/min、8.74/min±2.52/min。与正常对照组比较,模型组大鼠逃避潜伏期明显延长(P0.05),平均探索次数显著减少(P0.05);与模型组比较,补阳还五汤组、尼莫地平组大鼠逃避潜伏期明显缩短(P0.05),平均探索次数显著增加(P0.05)。光镜观察显示,补阳还五汤组和尼莫地平组均可见海马CA1区神经元脱失现象明显减轻,数目增多,神经元丢失率明显降低。结论补阳还五汤可以改善VD大鼠学习记忆能力,其机制可能与减轻脑缺血再灌注对海马CA1区神经元的损伤有关。 相似文献
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目的:观察补阳还五汤对血管性痴呆(VD)大鼠海马α-氨基羟甲基恶丙酸受体(AMPA)GluR1亚单位蛋白及mRNA表达的影响,探讨补阳还五汤治疗VD的机制。方法:四血管阻断法制备VD大鼠模型。设立假手术组、VD模型组、尼莫地平组(20mg·kg-1.d-1,灌胃30d)和补阳还五汤治疗组(50g·kg-1.d-1灌胃30d)。Morris水迷宫检测大鼠学习记忆能力的改变,免疫组化和Westernb lotting技术检测大鼠海马神经元GluR1蛋白的变化,实时荧光定量PCR技术检测大鼠海马GluR1mRNA表达的变化。结果:与假手术组相比,VD模型组大鼠逃避潜伏期延长和平均探索次数减少(P0.05);补阳还五汤明显改善了模型大鼠上述学习、记忆成绩(P0.05);假手术组、尼莫地平组与补阳还五汤治疗组之间差异无显著(P0.05)。VD模型组大鼠的GluR1蛋白及其mRNA表达水平较假手术组明显降低(P0.05);补阳还五汤治疗组大鼠海马的GluR1蛋白及其mRNA表达水平较模型组的表达明显升高(P0.05);假手术组、尼莫地平组与补阳还五汤治疗组之间差异无显著(P0.05)。结论:补阳还五汤可以改善VD大鼠学习记忆能力,其机制可能与减轻脑缺血再灌注对海马CA1区神经元的损伤及恢复海马组织GluR1蛋白及其mRNA的表达有关。 相似文献
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目的:探讨病例讨论式教学模式在病理生理学教学中的应用,并进行效果评价。方法:在2005级本科临床医学专业随机抽取2个大班(274人)作为实验组,1个大班(134人)作为对照组。实验组采用病例讨论式教学模式,对照组采用传统灌输式教学法。在学生中进行问卷调查并将期末考试成绩作对比。结果:在“对病理生理学课程的兴趣”等问题上两组存在明显的统计学差异,实验组的满意率高于对照组(P〈0.05);实验组的期末成绩分数和优秀率明显高于对照组(P〈0.05)。结论:采用病例讨论式的教学模式能增加学生学习兴趣,促进师生互动,帮助学生构建整体知识框架,培养学生临床思维能力。 相似文献
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Aim To explore the inhibitory effect of Buyang Huanwu Decoction on the inflammatory response in the hippocampus of brain tissues of CIRI rats by regulating SIRT1 and the underlying mechanism. Methods The middle cerebral artery embolization (MCAO) model was prepared in rats and divided into sham operation group (Sham), model group (MCAO/R), Buyang Huanwu Decoction group (BYHWT),and BYHWT + SIRT1 inhibitor group (BYHWT + EX527). Zea Longa was used to detect the neurological function score of rats in each group; TTC staining was used to determine the volume of cerebral infarction; HE staining was used to observe the pathological damage of the hippocampus; Western blot was used to detect the expression levels of SIRT1 and IL-6; immunohistochemistry was used to detect TNF-α, IL-1β expression level. Results Compared with the sham group,the neurological function score of the MCAO/R group increased (P < 0.05); the volume of cerebral infarction increased (P < 0.05); the nerve cells in hippocampus were severely damaged, arranged disorderly, and the nucleus was broken; Western blot showed that the expression of SIRT1 decreased, IL-6 expression increased (P <0.05); immunohistochemistry showed that TNF-α,IL-1β expression increased (P < 0.05). Compared with the MCAO/R group, the neurological function score of the BYHWT group decreased (P <0.05); the volume of cerebral infarction decreased (P < 0.05); the damage of nerve cells in hippocampus was reduced; Western blot showed that the expression of SIRT1 increased and IL-6 expression decreased (P < 0.05); immunohistochemistry showed that TNF-α, IL-1β expression decreased (P < 0.05). Compared with the BYHWT group, the neurological function score of the BYHWT + EX527 group increased (P < 0.05); the volume of cerebral infarction was raised (P <0.05); the damage of nerve cells in hippocampus was aggravated; Western blot showed that the expression of SIRT1 decreased and IL-6 expression increased (P < 0.05); immunohistochemistry showed that TNF-α, IL-1β expression increased (P < 0.05). Conclusions Preliminary discussion of Buyang Huanwu Decoction can activate SIRT1 in hippocampus of rat brain tissues to reduce the inflammatory response after CIRI and play a role in brain protection. © 2023 Publication Centre of Anhui Medical University. All rights reserved. 相似文献
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<正>微循环是血液与组织间进行物质交换的主要场所,由糖尿病相关因素导致的微循环结构和功能异常称为糖尿病微循环障碍。糖尿病肾病(diabetic nephropathy,DN)是糖尿病微循环障碍的表现之一,是慢性肾脏病变(chronic kidney disease,CKD)的一种重要类型,也是终末期肾衰竭(end-stage renal disease,ESRD)的主要原因。据统计,我国是世界上糖尿病患者人数最多的国家,其中2型糖尿病(diabetes mellitus type 2,T2DM)患者DN患病率为20%~40%,且呈逐年上升趋势[1]。微循环障碍是DN基本的病理基础,其可发生于糖尿病和糖尿病前期,早期对微循环障碍进行干预有助于防治DN[2],但糖尿病微循环障碍的发病机制尚未完全清楚。目前,糖尿病微循环障碍引起DN的作用机制尚未完全阐明,各项研究表明可能与能量代谢、氧化应激、自噬和炎症反应等有关。现将糖尿病微循环障碍及其引起DN的机制研究进展综述如下。 相似文献