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Aim To investigate the effects of baicalin on the inflammatory response and Toll-like receptor 4 (TLR4)/myeloid differentiation factor 88 (MyD 88)/nuclear factor kappa B (N F-K B) signaling pathway in Alzheimer' s disease (AD) rat model induced by lateral ventricular injection of streptozotocin (STZ). Methods The AD animal model was constructed by lateral ventricular injection of STZ in SD rats, and divided into sham operation group, model group, low-dose (60 mg -1 • kg-1 • d-1 ) baicalin group, high-dose (120 mg-1 • kg-1 • d-1 ) baicalin group and minocycline group (36 mg-1 • kg-1 • d-1 ). The learning and memory ability of rats were assessed by Morris water maze. The mRNA expressions of tumor necrosis Factor-α(TNF-α), interleukin-6 (IL-6), interleukin-1β(IL-1β) were detected by real-time quantitative PCR, the protein expressions of TLR4, MyD88, N F-Κ B p65, p-NF-κB p65 and nucleus/cytoplasm NF-ΚB p65 were detected by Western blot, and NF-ΚB p65 transfering from cytoplasm to nucleus and the activation of microglia were measured by immunofluorescence. Results Compared with the sham operation group, animals in the model group showed decreased learning and memory capacity, increased mRNA expression of TNF-α, IL-6 and IL-1κ, up-regulated protein expressions of TLR4 and MyD88, the ratio of p-NF-κB p65/NF-κB p65 and the nucleus/cytoplasm ratio of NF-ΚB p65, enhanced expression of NF-KB p65 in nucleus and the activation of microglias. Compared with the model group, baicalin group and minocycline group improved the learning and memory capacity of AD rats, decreased the mRNA expression of TNF-α, IL-6 and IL-1β, down-regulated the protein expressions of TLR4 and MyD88, the p-NF-ΚB P65/NF-KB p65 ratio and the nucleus/cytoplasm ratio of NF-KB p65, and reduced the expression of NF-KB p65 in nucleus and the activation of microglias. Conclusion Baicalin may exert neuroprotective effects by inhibiting the TLR4/MyD88/NF-KB signaling pathway and neuroinflammation response in the AD brain. © 2023 Publication Centre of Anhui Medical University. All rights reserved.  相似文献   
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目的分析大邑县2011年传染病疫情特征,为有效防治传染病提供科学依据。方法应用描述性流行病学方法对大邑县2011年法定报告传染病疫情资料进行统计分析。结果 2011年共报告乙丙类传染病16种,179例,报告发病率为268.79/10万,病死率为0.65/10万,流行性腮腺炎、手足口病、肺结核、梅毒、丙肝发病数位居前5位。结论今后大邑县的传染病防治工作应当加强对流行性腮腺炎、手足口病、肺结核、梅毒、丙肝等多发病、重点疾病的预防控制,并加强对幼儿、学生、农民、学校等重点职业(人群)和场所的传染病防控制工作。  相似文献   
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目的为法定传染病的准确诊断和报告提供科学依据。方法对2012年有慢性乙肝、丙肝、隐性梅毒、其他感染性腹泻报告的医疗机构进行现场调查。结果慢性乙肝、丙肝、隐性梅毒、其他感染性腹泻的诊断符合率分别为62.50%,62.96%,69.57%,60.53%。结论应当加强医务人员对传染病诊断标准的培训和学习,疾控和医疗机构不仅要注重传染病报告的及时率、漏报率,更要注重报告的准确性。  相似文献   
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目的:探讨当归芍药散对阿尔茨海默病(AD)大鼠线粒体形态和功能的影响及作用机制。方法:采用双侧侧脑室注射链脲佐菌素(STZ)构建AD模型大鼠。40只大鼠随机分为假手术组、模型组、当归芍药散低、中、高剂量(12、24、36 g·kg-1)组,连续灌胃14 d后透射电镜观察大鼠海马区线粒体形态变化,原位末端标记法(TUNEL)检测细胞凋亡情况,免疫荧光检测活性氧(ROS)、过氧化物酶体增殖物激活受体γ辅激活因子-1α(PGC-1α)的表达,实时荧光定量聚合酶链式反应(Real-time PCR)检测线粒体动力相关蛋白1(Drp1)、线粒体融合蛋白2(MFN2)、细胞色素C氧化酶亚基Ⅳ(COXⅣ)、PGC-1α mRNA的表达,蛋白免疫印迹法(Western blot)检测腺苷酸活化蛋白激酶(AMPK)、磷酸化腺苷酸活化蛋白激酶(p-AMPK)、沉默信息调节因子1(SIRT1)、PGC-1α蛋白的表达。结果:与假手术组比较,模型组大鼠海马区线粒体损伤明显,ROS产生和细胞凋亡率显著增高(P<0.01),MFN2、COXⅣ、PGC-1α mRNA表达显著下调,Drp...  相似文献   
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基于PINK1-Parkin信号通路,探讨当归芍药散对链脲佐菌素(streptozocin, STZ)诱导的阿尔茨海默病(Alzheimer′s disease, AD)大鼠模型线粒体自噬影响的作用机制。通过双侧侧脑室注射STZ构建AD大鼠模型,实验分为正常组、模型组、当归芍药散低剂量组(12 g·kg-1·d-1)、当归芍药散中剂量组(24 g·kg-1·d-1)、当归芍药散高剂量组(36 g·kg-1·d-1)。Morris水迷宫实验检测大鼠学习记忆功能,透射电镜和免疫荧光共定位检测线粒体自噬情况,免疫印迹法(Western blot)检测PTEN诱导的激酶1 (PTEN induced putative kinase 1,PINK1)、Parkin、LC3BⅠ/LC3BⅡ、p62蛋白的表达。与正常组比较,模型组大鼠学习记忆功能显著降低(P<0.01),PINK1、Parkin表达降低(P<0.05),而LC3BⅠ/LC3BⅡ、p62表达显...  相似文献   
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目的 研究当归芍药散对β淀粉样蛋白1-42(Aβ1-42)诱导的阿尔茨海默症(Alzheimer’s Disease,AD)模型大鼠神经炎症及Toll样受体4(TLR4)/髓样分化因子(MyD88)/核因子-κB(NF-κB)信号通路的调控作用。方法 SD大鼠大脑双侧侧脑室注射Aβ1-42构建AD动物模型。实验分为假手术组、模型组、当归芍药散组和阳性药物组。假手术组、模型组给予生理盐水灌胃,当归芍药散组给予当归芍药散24 g·kg-1·d-1灌胃,阳性药物组给予米诺环素36 mg·kg-1·d-1灌胃,连续灌胃14 d。Morris水迷宫实验测定大鼠的学习记忆能力。复制模型成功后取材,HE染色检测海马神经元组织病理形态学变化,免疫荧光法检测小胶质细胞和星形胶质细胞活化情况,实时荧光定量PCR(qPCR)检测炎症因子白细胞介素1β(IL-1β)、白细胞介素6(IL-6)、肿瘤坏死因子α(TNF-α)的mRNA表达情况,免疫印迹法(W...  相似文献   
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