目的:通过观察藏红花酸对肝纤维化小鼠肝组织病理学改变及p38MAPK蛋白表达的影响,探讨其抗肝纤维化作用及可能的机制。方法:36只6周龄雄性昆明小鼠随机分为3组:藏红花酸组、模型组、正常组。除正常对照组外,其余两组小鼠给予30%四氯化...目的:通过观察藏红花酸对肝纤维化小鼠肝组织病理学改变及p38MAPK蛋白表达的影响,探讨其抗肝纤维化作用及可能的机制。方法:36只6周龄雄性昆明小鼠随机分为3组:藏红花酸组、模型组、正常组。除正常对照组外,其余两组小鼠给予30%四氯化碳橄榄油溶液腹腔注射,首次注射5 m L/Kg,以后每次3 m L/Kg,每3日1次,连续12周。同时藏红花酸组给予藏红花酸5mg/Kg灌胃,每日1次,连续12周。实验过程中,观察各组小鼠的一般状态。12周末处死小鼠,肝组织切片行HE、Masson染色,显微镜下观察病理改变,免疫组化检测小鼠肝组织p38MAPK蛋白的表达。结果:实验过程中,模型组小鼠一般状态较差,体重增长缓慢;藏红花酸组小鼠一般状态尚可,体重较模型组增长明显(P<0.05)。肝组织HE、Masson染色结果显示:模型组小鼠肝纤维化程度较重(造模成功),与其相比,藏红花酸组小鼠肝纤维化程度有所改善,差异有统计学意义。与模型组相比,藏红花酸组肝组织p38MAPK表达显著下降(P<0.05)。结论:藏红花酸能有效减轻小鼠肝损伤及纤肝维化程度,其抗肝纤维化的机制可能与下调p38MAPK蛋白的表达有关。展开更多
Uncontrolled and chronic microglia activation has been implicated in the process of dopaminergic neuron degeneration in sporadic Parkinson＇s disease （PD）. Elevated proinflammatory mediators, presumably from activat...Uncontrolled and chronic microglia activation has been implicated in the process of dopaminergic neuron degeneration in sporadic Parkinson＇s disease （PD）. Elevated proinflammatory mediators, presumably from activated microglia （e.g., cytokines, PGE2, nitric oxide, and superoxide radical）, have been observed in PD patients and are accompanied by dopaminergic neuronal loss. Preclinical studies have demonstrated the deleterious effects of proinflammatory mediators in various in vivo and in vitro models of PD. The use of in vitro studies provides a unique tool to investigate the interaction between neurons and microglia and is especially valuable when considering the role of activated microglia in neuronal death. Here we summarize findings highlighting the potential mechanisms of microglia- mediated neurodegeneration in PD.展开更多
文摘目的:通过观察藏红花酸对肝纤维化小鼠肝组织病理学改变及p38MAPK蛋白表达的影响,探讨其抗肝纤维化作用及可能的机制。方法:36只6周龄雄性昆明小鼠随机分为3组:藏红花酸组、模型组、正常组。除正常对照组外,其余两组小鼠给予30%四氯化碳橄榄油溶液腹腔注射,首次注射5 m L/Kg,以后每次3 m L/Kg,每3日1次,连续12周。同时藏红花酸组给予藏红花酸5mg/Kg灌胃,每日1次,连续12周。实验过程中,观察各组小鼠的一般状态。12周末处死小鼠,肝组织切片行HE、Masson染色,显微镜下观察病理改变,免疫组化检测小鼠肝组织p38MAPK蛋白的表达。结果:实验过程中,模型组小鼠一般状态较差,体重增长缓慢;藏红花酸组小鼠一般状态尚可,体重较模型组增长明显(P<0.05)。肝组织HE、Masson染色结果显示:模型组小鼠肝纤维化程度较重(造模成功),与其相比,藏红花酸组小鼠肝纤维化程度有所改善,差异有统计学意义。与模型组相比,藏红花酸组肝组织p38MAPK表达显著下降(P<0.05)。结论:藏红花酸能有效减轻小鼠肝损伤及纤肝维化程度,其抗肝纤维化的机制可能与下调p38MAPK蛋白的表达有关。
文摘Uncontrolled and chronic microglia activation has been implicated in the process of dopaminergic neuron degeneration in sporadic Parkinson＇s disease （PD）. Elevated proinflammatory mediators, presumably from activated microglia （e.g., cytokines, PGE2, nitric oxide, and superoxide radical）, have been observed in PD patients and are accompanied by dopaminergic neuronal loss. Preclinical studies have demonstrated the deleterious effects of proinflammatory mediators in various in vivo and in vitro models of PD. The use of in vitro studies provides a unique tool to investigate the interaction between neurons and microglia and is especially valuable when considering the role of activated microglia in neuronal death. Here we summarize findings highlighting the potential mechanisms of microglia- mediated neurodegeneration in PD.
