支气管哮喘病因病理及防治进展

综述了支气管哮喘的病因病理研究和临床防治方面的进展，以探讨降低哮喘患病率及死亡率的可能途径。     

β-淀粉样蛋白诱导大鼠海马S100β表达的作用及机制

目的　探讨 β 淀粉样蛋白 (Aβ)对S10 0 β表达的影响及作用机制。 方法　采用Aβ2 5-3 5和IL 1ra ,选择大鼠海马CA1区进行定位注射 ,通过行为学测试、刚果红染色和免疫组化技术结合图像分析的方法 ,对不同时间大鼠的学习记忆、淀粉样沉积、GFAP和海马CA1区S10 0 β表达的变化进行观测。 结果　Aβ2 5-3 5注射后 ,大鼠的学习记忆能力明显下降 ;海马CA1区出现Aβ沉积 ,并有大量GFAP阳性胶质细胞包绕 ;实验组S10 0 β阳性细胞数目在 3、7、2 1d较对照组均有明显增多 ,细胞平均面积只在 2 1d才有明显增大。脑内注射IL 1ra后 3、7d,S10 0 β阳性细胞数目明显低于同组的Aβ大鼠 ,而高于对照组。结论　Aβ2 5-3 5脑内注射可建立具有类似阿尔茨海默病的局部病理改变和学习记忆损害的AD动物模型 ;Aβ2 5-3 5可上调大鼠海马CA1区S10 0 β的表达 ,实验早期以S10 0 β阳性细胞的数目增加为主 ,后期表现为细胞体积的增大 ;IL 1ra脑内注射可明显降低Aβ2 5-3 5上调S10 0 β表达的作用 ,其机制是阻断由Aβ2 5-3 5激活的小胶质细胞释放的IL 1对星形胶质细胞的活化作用。     

Screening of chemokine receptor CCR4 antagonists by capillary zone electrophoresis

Abstract CC chemokine receptor 4 （CCR4） is a kind of G-protein-coupled receptor, which plays a pivotal role in allergic inflammation. The interaction between 2-（2-（4-chloro-phenyl）-5-{[（naphthalen-1- y...     

Inhibitory effects of microinjection of morphine into thalamic nucleus submedius on ipsilateral paw bee venom-induced inflammatory pain in the rat

Objective To examine whether microinjectlon of morphine into the rat thaiamle nucleus submedlus (Sin) could depress the bee venom (BV)-induced nociceptive behaviours. Methods In inflammatory pain model induced by BV subcutaneous injection into rat unilateral hind paw, the inhibitory effects of morphine microinjection into thalamic nucleus suhmedius (Sin) on the spontaneous nociecptlve behavior, heat hyperalgesia and tactile ailodynia, and the influence of naioxone on the morphine effects were observed in the rat. Results A single dose of morphine (5.0 μg, 0. 5μL) applied into the Sm ipsilaterni to the BV injected paw significantly depressed the spontaneous paw flinching response. Morphine also significantly increased the heat paw withdrawal iateneies in the bilateral hind paw and the tactile paw withdrawal threshold in the ipsilnteral hind paw 2 hours after BV injection. All these depressive effects could be effectively antagonized by pre-treatment with the opiuld receptor antagonist naloxone (1.0μg, 0. 5μL) in the Sm 5rain prior to morphine administration. Naloxone alone injected to the Sm had no effect on the BV-induecd nociceptive behavior. Conclusion These results suggest that Sm is involved in opioid receptor-mediated antt-nociception in the rat with the BV-induced inflammatory pain. Together with results from previous studies, it is likely that this effect is produced by activation of the Sm-ventrolateral orbital cortex-periaqueductal gray pathway, leading to activation of the brainstem descending inhibitory system and depression of the nodceptive inputs at the spinal cord level.     

AT2对成年压力超负荷性肥大心肌细胞TNFα、IL-1β及IL-6分泌的调控

目的 观察AT2对肥大心肌细胞炎症因子合成的调控作用及AT1和AT2间的相互关系.方法 采用腹主动脉缩窄法构建SD大鼠压力超负荷性心肌肥大模型.选用术后8周肥大的心肌细胞,将其分为AngⅡ组、AngⅡ losartan组、AngⅡ PD123319及AngⅡ losartan PD123319组.待实验结束,RT-PCR法检测细胞TNFα、IL-1β及IL-6的mRNA表达水平,放免法检测TNFα、IL-1β及IL-6的蛋白表达.结果 与AngⅡ组相比,AT1拮抗剂losartan不影响TNFα和IL-1β的mRNA及蛋白表达.单独应用AT2拮抗剂PD123319及联合应用losartan和PD123319均可使TNFα和IL-1β的mRNA及蛋白表达水平下调.联合应用二者TNFα和IL-1β mRNA的表达水平介于单独应用losartan和PD123319组之间.与AngⅡ单独联用losartan或PD123319相比,同时联用二者可使IL-6 mRNA的表达水平上调.结论 AT2参与了肥大心肌细胞炎症因子的表达调控.AT1与AT2之间并非简单的拮抗关系.