目的观察大鼠局灶性脑缺血/再灌注后丝裂原活化蛋白激酶家族中JNK1/2(c-Jun氨基末端激酶1/2)的活化情况以及银杏叶提取物Egb761对其影响。方法雄性成年SD大鼠随机分成3组(n=5):假手术组、生理盐水对照组和Egb761组。分别于缺血前6天每...目的观察大鼠局灶性脑缺血/再灌注后丝裂原活化蛋白激酶家族中JNK1/2(c-Jun氨基末端激酶1/2)的活化情况以及银杏叶提取物Egb761对其影响。方法雄性成年SD大鼠随机分成3组(n=5):假手术组、生理盐水对照组和Egb761组。分别于缺血前6天每天用生理盐水4 m l和Egb761 150 mg/kg(Egb761用4 m l生理盐水溶解)灌胃。采用线栓法致大脑中动脉栓塞(MCAO)模型,在脑缺血再灌注后处死大鼠,对缺血侧海马进行免疫印迹法检测JNK1/2磷酸化水平。结果局灶脑缺血/再灌注可以诱导JNK1/2激活,30 m in达第1个高峰,3天达第2个高峰;Egb761可显著抑制脑缺血再灌注后JNK1/2的激活(P<0.05),JNK1/2的蛋白表达量在以上不同处理条件下没有明显变化。结论局灶性脑缺血再灌注可诱导缺血侧海马JNK1/2活化,Egb761干预可使缺血侧海马JNK1/2活化受到抑制,减轻缺血侧海马的损伤。展开更多
Recent research shows that the JNK1/2 signaling pathway plays a neuroprotective role against ischemia-reperfusion injury by cross-talk with other pathways.The present study investigated the effects of isoflurane and s...Recent research shows that the JNK1/2 signaling pathway plays a neuroprotective role against ischemia-reperfusion injury by cross-talk with other pathways.The present study investigated the effects of isoflurane and sevoflurane postconditioning on JNK1/2 pathway activity and neuronal cell viability after oxygen and glucose deprivation injury in hippocampal slices in vitro.Techniques used included population spike analysis,propidium iodide fluorescent staining,western blot assay,and the use of JNK1/2-specific pharmacological tools such as anisomycin （agonist） and SP600125 （inhibitor）.We found that both isoflurane and sevoflurane inhibited JNK pathway activity and had neuroprotective effects against oxygen and glucose deprivation injury in slices of rat hippocampus in vitro.Postconditioning with volatile anesthetics exerted neuroprotective effects on nerve cells and preserved the function of the CA1 region by inhibiting JNK1/2 phosphorylation.This suppression of JNK1/2 activity could underlie the observed synergistic neuroprotective effect produced by volatile anesthetic postconditioning.展开更多
目的探讨香烟烟雾对哮喘大鼠肺组织内皮素2(ET-2)表达的影响。方法大鼠腹腔注射鸡卵清蛋白/Al(OH)3混合液1 m L致敏建立哮喘模型(哮喘模型组,n=6),在哮喘模型组基础上烟熏(10支/d)连续4周为香烟烟雾哮喘组(烟雾哮喘组,n=6),分别以地塞米...目的探讨香烟烟雾对哮喘大鼠肺组织内皮素2(ET-2)表达的影响。方法大鼠腹腔注射鸡卵清蛋白/Al(OH)3混合液1 m L致敏建立哮喘模型(哮喘模型组,n=6),在哮喘模型组基础上烟熏(10支/d)连续4周为香烟烟雾哮喘组(烟雾哮喘组,n=6),分别以地塞米松2 mg/(kg·d)腹腔注射1周、ET受体抑制剂波生坦100 mg/(kg·d)灌胃及联合处理分为地塞米松处理组、波生坦处理组、地塞米松及波生坦处理组,每组6只,设正常对照(正常对照组,腹腔注射生理盐水1 m L,n=6)及香烟烟雾对照[在正常对照组基础上,连续烟熏(10支/d)4周,n=6]。收集左肺上叶支气管肺泡灌洗液(BALF)检测细胞计数及分类,右肺上叶HE染色观察肺组织病理学改变;其余肺组织行Western blot法及免疫组织化学染色法分别检测肺组织c-Jun氨基末端激酶1/2(JNK1/2)、ET-2蛋白水平,硫代巴比妥酸法测丙二醛(MDA)水平,微量酶标法测谷胱甘肽(GSH)水平。结果与对照组比较,香烟烟雾对照组、哮喘模型组、香烟烟雾哮喘组BALF中白细胞数、中性粒细胞数及嗜酸性粒细胞数升高,肺组织中ET-2蛋白、JNK1/2蛋白、MDA及GSH水平升高;而与香烟烟雾哮喘组比较,地塞米松处理组、波生坦处理组、地塞米松及波生坦处理组BALF中白细胞数、中性粒细胞数及嗜酸性粒细胞数均降低。肺组织中ET-2蛋白、JNK1/2蛋白、MDA及GSH表达降低。地塞米松处理组、波生坦处理组、地塞米松及波生坦处理组气道炎症均有改善,地塞米松及波生坦处理组改善最明显。ET-2在地塞米松处理组、波生坦处理组、地塞米松及波生坦处理组肺组织染色强度减少,地塞米松及波生坦处理组染色强度减少更明显。结论香烟烟雾暴露可加重哮喘大鼠气道炎症,ET受体抑制剂波生坦可改善气道炎症,香烟烟雾暴露哮喘发生的炎症机制可能与ET-2及JNK1/2通路有关。展开更多
文摘目的观察大鼠局灶性脑缺血/再灌注后丝裂原活化蛋白激酶家族中JNK1/2(c-Jun氨基末端激酶1/2)的活化情况以及银杏叶提取物Egb761对其影响。方法雄性成年SD大鼠随机分成3组(n=5):假手术组、生理盐水对照组和Egb761组。分别于缺血前6天每天用生理盐水4 m l和Egb761 150 mg/kg(Egb761用4 m l生理盐水溶解)灌胃。采用线栓法致大脑中动脉栓塞(MCAO)模型,在脑缺血再灌注后处死大鼠,对缺血侧海马进行免疫印迹法检测JNK1/2磷酸化水平。结果局灶脑缺血/再灌注可以诱导JNK1/2激活,30 m in达第1个高峰,3天达第2个高峰;Egb761可显著抑制脑缺血再灌注后JNK1/2的激活(P<0.05),JNK1/2的蛋白表达量在以上不同处理条件下没有明显变化。结论局灶性脑缺血再灌注可诱导缺血侧海马JNK1/2活化,Egb761干预可使缺血侧海马JNK1/2活化受到抑制,减轻缺血侧海马的损伤。
基金the Natural Science Foundation of Shihezi University,No.RCZX200688
文摘Recent research shows that the JNK1/2 signaling pathway plays a neuroprotective role against ischemia-reperfusion injury by cross-talk with other pathways.The present study investigated the effects of isoflurane and sevoflurane postconditioning on JNK1/2 pathway activity and neuronal cell viability after oxygen and glucose deprivation injury in hippocampal slices in vitro.Techniques used included population spike analysis,propidium iodide fluorescent staining,western blot assay,and the use of JNK1/2-specific pharmacological tools such as anisomycin （agonist） and SP600125 （inhibitor）.We found that both isoflurane and sevoflurane inhibited JNK pathway activity and had neuroprotective effects against oxygen and glucose deprivation injury in slices of rat hippocampus in vitro.Postconditioning with volatile anesthetics exerted neuroprotective effects on nerve cells and preserved the function of the CA1 region by inhibiting JNK1/2 phosphorylation.This suppression of JNK1/2 activity could underlie the observed synergistic neuroprotective effect produced by volatile anesthetic postconditioning.
文摘目的探讨香烟烟雾对哮喘大鼠肺组织内皮素2(ET-2)表达的影响。方法大鼠腹腔注射鸡卵清蛋白/Al(OH)3混合液1 m L致敏建立哮喘模型(哮喘模型组,n=6),在哮喘模型组基础上烟熏(10支/d)连续4周为香烟烟雾哮喘组(烟雾哮喘组,n=6),分别以地塞米松2 mg/(kg·d)腹腔注射1周、ET受体抑制剂波生坦100 mg/(kg·d)灌胃及联合处理分为地塞米松处理组、波生坦处理组、地塞米松及波生坦处理组,每组6只,设正常对照(正常对照组,腹腔注射生理盐水1 m L,n=6)及香烟烟雾对照[在正常对照组基础上,连续烟熏(10支/d)4周,n=6]。收集左肺上叶支气管肺泡灌洗液(BALF)检测细胞计数及分类,右肺上叶HE染色观察肺组织病理学改变;其余肺组织行Western blot法及免疫组织化学染色法分别检测肺组织c-Jun氨基末端激酶1/2(JNK1/2)、ET-2蛋白水平,硫代巴比妥酸法测丙二醛(MDA)水平,微量酶标法测谷胱甘肽(GSH)水平。结果与对照组比较,香烟烟雾对照组、哮喘模型组、香烟烟雾哮喘组BALF中白细胞数、中性粒细胞数及嗜酸性粒细胞数升高,肺组织中ET-2蛋白、JNK1/2蛋白、MDA及GSH水平升高;而与香烟烟雾哮喘组比较,地塞米松处理组、波生坦处理组、地塞米松及波生坦处理组BALF中白细胞数、中性粒细胞数及嗜酸性粒细胞数均降低。肺组织中ET-2蛋白、JNK1/2蛋白、MDA及GSH表达降低。地塞米松处理组、波生坦处理组、地塞米松及波生坦处理组气道炎症均有改善,地塞米松及波生坦处理组改善最明显。ET-2在地塞米松处理组、波生坦处理组、地塞米松及波生坦处理组肺组织染色强度减少,地塞米松及波生坦处理组染色强度减少更明显。结论香烟烟雾暴露可加重哮喘大鼠气道炎症,ET受体抑制剂波生坦可改善气道炎症,香烟烟雾暴露哮喘发生的炎症机制可能与ET-2及JNK1/2通路有关。
