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作 者:王翔[1] 何平[1] 王微[1] 赵浩淼[1] 易省阳[1] 王春蝶 WANG Xiang;HE Ping;WANG Wei;ZHAO Haomiao;YI Shengyang;WANG Chundie(Emergency Center,Hainan General Hospital&Hainan Affiliated Hospital of Hainan Medical University,Haikou 570100,China;Health Center,Hainan General Hospital&Hainan Affiliated Hospital of Hainan Medical University,Haikou 570100,China)
机构地区:[1]海南省人民医院海南医学院附属海南医院急救中心,海口570100 [2]海南省人民医院海南医学院附属海南医院保健中心,海口570100
出 处:《免疫学杂志》2020年第9期770-776,共7页Immunological Journal
基 金:海南省重点研发计划(ZDYF2017067)。
摘 要:目的探讨绿原酸(CGA)减轻脓毒症模型大鼠肺组织损伤的可能机制。方法利用盲肠结扎穿孔法(CLP)构建脓毒症大鼠模型,并用5、10、15 mg/kg的CGA和15 mg/kg的丙酮酸乙酯(EP)静脉给药6 h,比较各组大鼠7 d生存率、肺湿干质量比(W/D)、肺组织病理变化、肺组织细胞凋亡率、凋亡蛋白表达量、血清炎症因子、肺组织氧化应激指标、肺组织Nrf2通路关键蛋白表达情况。结果CGA干预后提高了大鼠7 d存活率,促进了肺组织中SOD水平、Bcl-2、Nrf2、HO-1、NQO1蛋白表达量,降低了W/D、肺组织细胞凋亡率、Bax表达水平、血清TNF-α、IL-1β、IL-6水平以及肺组织中MDA水平。结论CAG可能通过激活Nrf2信号通路,改善氧应激反应,减少炎症因子及自由基生成,减轻脓毒症大鼠炎症反应。The article was performed to explore the possible mechanism of chlorogenic acid(CGA)alleviating lung tissue injury in sepsis model rats.The cecal ligation and puncture(CLP)was applied to construct sepsis rat models.Then the They rats were given intravenous administration of 5,10 and 15 mg/kg CGA,and 15 mg/kg ethyl pyruvate(EP)for 6 h.Related indexes were detected and compared,including 7-day survival rate,the ratio of wet to dry weight(W/D)of lung,the pathological changes of lung tissue,the apoptosis rate of lung tissue,the expression quantities of apoptosis proteins,serum inflammatory factors,the oxidative stress indexes of lung tissue,the expression of Nrf2 pathway key protein in lung tissue.Data showed that after CGA intervention,the 7-day survival rate,the level of SOD in lung tissue,the expression quantities of Bcl-2,Nrf2,HO-1 and NQO1 proteins were increased,but the W/D rate,the apoptosis rate of lung tissue,the expression level of Bax,the levels of serum TNF-α,IL-1βand IL-6 levels,and MDA in lung tissue were decreased.In conclusion,CAG may improve oxygen stress response,reduce production of inflammatory factors and free radicals,and alleviate inflammatory response in sepsis rats by activating Nrf2 signaling pathway.
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