大黄对MCAO模型大鼠的神经保护作用

目的研究大黄提取物对MCAO模型大鼠的神经保护作用,并探讨其作用机制。方法SPF级雄性SD大鼠45只,随机分为sham组、MCAO组、MCAO+大黄组,线栓法制备MCAO模型,大黄提取物给药浓度为200 mg·kg^-1·d^-1,连续给药6 d,尼氏染色法检测尼氏体的表达,免疫荧光法检测大鼠缺血侧NeuN、NF200的表达,RT-qPCR法检测Egr1、Egr2、Egr4 mRNA表达,Western blot检测NGF及BDNF蛋白的表达。结果与MCAO组相比,大黄提取物作用后,尼氏染色法检测结果表明大黄提取物可以减少MCAO模型大鼠脑梗死面积,免疫荧光检测结果表明大黄提取物可以升高MCAO模型大鼠缺血侧NeuN、NF200的表达;经RT-qPCR检测,大黄提取物能够提高Egr1、Egr2、Egr4 mRNA基因表达;经Western blot检测,大黄提取物能够提高NGF及BDNF蛋白的表达。结论大黄提取物能够改善MCAO模型大鼠缺血侧神经元存活环境,具有神经保护作用。     

红景天苷调控PI3K/Akt信号通路对永久性脑缺血大鼠的保护作用

目的研究红景天苷(salidroside,Sal)通过调控PI3K/AKT信号通路对永久性大脑中动脉闭塞模型(pMCAO)大鼠的神经保护作用及其机制。方法健康成年雄性SPF级雄性SD大鼠70只,其中30只大鼠随机分为假手术组(sham组)、模型组(pMCAO组)、红景天苷给药组(pMCAO+Sal组),线栓法造模成功后,对sham组和pMCAO组大鼠腹腔注射生理盐水,pMCAO+Sal组按照50 mg·kg^-1·d^-1腹腔注射红景天苷(50 mg·kg^-1·d^-1),给药1 d。40只大鼠随机分为假手术组(sham组)、模型组(pMCAO组)、红景天苷给药组(pMCAO+Sal组)、抑制剂组(pMCAO+Sal+LY组);侧脑室注射PI3K抑制剂30 min后,制备pMCAO模型,1 h后腹腔注射红景天苷,给药1 d。免疫组织化学染色测定脑组织中NeuN表达,Western blot分析脑组织中NeuN蛋白、NF-κBp50核蛋白的表达,RT-qPCR检测IL-6和TNF-α的表达。结果与pMCAO组比较,红景天苷作用后,NeuN免疫荧光染色表达量明显增加,且能够促进NeuN蛋白,抑制NF-κB p50核蛋白及IL-6和TNF-αmRNA表达。经PI3K抑制剂LY294002作用后,红景天苷对上述指标作用不明显。结论红景天苷能够通过调控PI3K/AKT信号通路,抑制NF-κB p50核转录水平,进而抑制炎症因子,对pMCAO模型大鼠具有神经保护的作用。     

贺氏三通法治疗鼻鼽1则

介绍临床采用贺氏三通法针灸治疗鼻鼽验案1则。贺氏三通法针灸治疗能有效治疗鼻鼽,急性期宣肺泄热,祛风通窍而缓解鼻鼽症状,近期疗效显著;慢性期扶正固本,温补肺肾,预防鼻鼽发作,标本兼顾。     

植入CIED患者选择社区随访的影响因素及其效果初探

目的探讨植入心脏植入式电子器械(CIED)患者选择社区随访的影响因素及其效果。方法该研究为前瞻性队列研究。入选2021年2月至2022年2月在上海交通大学医学院附属同仁医院心内科CIED门诊及其签约的10家社区卫生服务中心进行随访的植入了CIED的患者。在CIED门诊进行随访的患者纳入常规门诊随访组, 有1次及以上社区卫生服务中心随访经历的患者纳入社区随访组。社区随访组与常规门诊随访组按照1∶3的比例进行匹配。通过问卷调查收集入选患者的基线临床资料, 问卷由基本情况、随访情况、社区医疗情况3方面内容组成。通过CarelinkExpress电子随访平台及同仁医院CIED门诊信息系统提取患者随访相关数据。随访时调整了治疗方案或CIED参数定义为采取行动的随访(VWA), 社区随访时发生了转诊也定义为VWA。随访终点为发生主要不良事件。采用多因素logistic回归模型分析患者选择社区随访的影响因素。结果共入选患者132例, 其中社区随访组33例, 男性16例(48.5%), 年龄(79.5±8.0)岁;常规门诊随访组99例, 男性48例(48.5%), 年龄(80.8±7.2)岁。两组患者...     

乙酰半胱氨酸联合琥乙红霉素治疗儿童重症支原体肺炎的临床研究

目的 探讨乙酰半胱氨酸联合琥乙红霉素治疗儿童重症支原体肺炎的临床疗效。方法 选取2020年1月—2021年12月在唐山市妇幼保健院诊治的106例肺炎患儿,随机分为对照组和治疗组,每组各53例。对照组口服琥乙红霉素颗粒,每次7.5～12.5 mg/kg,4次/d。在对照组的基础上,治疗组雾化吸入吸入用乙酰半胱氨酸溶液,3 mL/次,2次/d。两组用药10 d观察治疗效果。观察两组患者临床疗效,比较治疗前后两组患者症状改善时间,血气指标血氧饱和度(SaO₂)、动脉血氧分压(pO₂)和动脉血二氧化碳分压(pCO₂),白细胞介素-6(IL-6)、降钙素(PCT)、肿瘤坏死因子-α(TNF-α)和γ干扰素(IFN-γ)水平,及不良反应情况。结果 治疗后,治疗组临床有效率为98.11%,明显高于对照组(83.02%,P<0.05)。经治疗,治疗组症状改善时间均早于对照组(P<0.05)。治疗后,两组SaO₂、pO₂指标明显高于治疗前,pCO₂指标明显低于治...     

The neuroprotective effect of salidroside prophylactic administration on MCAO model rats北大核心CSCD

Aim To investigate the neuroprotective effect of prophylactic administration of salidroside (Sal) on MCAO rats. Methods A total of 52 SD adult male rats were randomly divided into sham operation group (Sham), model group (MCAO) and salidroside pre-administration group (MCAO + Sal). The dose of Sal was 50 mg·kg-1. MCAO model was administered by continuous intraperitoneal injection for 7 days, followed by the wire embolization 0.5 h after the 7th day of administration, and the materials were taken 24 h after anesthesia. TTC staining was used to detect the volume of cerebral infarction in rats, TUNEL staining was used to detect the number of nerve cell apoptosis, Western blot was used to detect the expression of Bax, Bcl-2, cleaved Caspase-3 and total Caspase-3 proteins, naphthol AS-D chloroacetate was used to detect the expression of neutrophils in brain tissues, RT-qPCR was used to detect the mRNA expression of IL-1β, IL-6 and TNF-α, and immunofluorescence staining was used to determine the expression of NeuN in brain tissues. Results Pre-administration of salidroside for seven days significantly reduced cerebral infarct volume and nerve cell apoptosis in MCAO rats, promoted the expression of Bcl-2 protein, inhibited the expression of Bax and cleaved Caspase-3 proteins, but it had no significant effect on total Caspase-3 protein, and it reduced the recruitment of neutrophils in ischemic brain tissues, decreased the mRNA expression of inflammatory factors IL-1β, IL-6, TNF-α, and up-regulated the expression of NeuN. Conclusions Pre-administration of salidroside for seven days can significantly reduce the volume of cerebral infarction in MCAO rats, inhibit nerve cell apoptosis, reduce inflammation and promote the expression of NeuN, then playing a neuroprotective role. © 2023 Publication Centre of Anhui Medical University. All rights reserved.