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作 者:毛亚男 佟昌慈 尹凤先[1] MAO Ya-nan;TONG Chang-ci;YIN Feng-xian(Department of Respiratory,Daxing District People's Hospital of Beijing,Beijing 102600;Shuren International College,Shenyang Medical College,Shenyang 110034,China)
机构地区:[1]北京市大兴区人民医院呼吸科,北京102600 [2]沈阳医学院树人国际学院,辽宁沈阳110034
出 处:《解剖科学进展》2024年第1期79-81,85,共4页Progress of Anatomical Sciences
摘 要:目的探讨CaMKK2是否通过调控AMPK通路减轻肺缺血再灌注损伤。方法45只8周龄健康雄性C57BL/6小鼠随机分为假手术组(Sham组)、肺缺血再灌注组(IR组)和IR+CaMKK2抑制剂组(CaMKK2inhibitor组),每组15只,建立缺血再灌注诱导的肺缺血再灌注损伤(LIRI)小鼠模型,通过生存分析评价小鼠存活率,血气分析评价小鼠呼吸功能,肺湿干重比评价肺水肿,HE染色评价肺组织病理情况,Westernblot实验分析肺组织NF-κB、TNF-α及CaMKK2/AMPK/mTOR信号通路蛋白表达。结果抑制CaMKK2会增加LIRI导致的小鼠死亡率,加重肺水肿和呼吸功能障碍(P<0.05),增加肺组织炎细胞浸润,增加肺组织炎症蛋白NF-κB和TNF-α的表达,加重LIRI导致的磷酸化AMPK减少和磷酸化mTOR的增多(P<0.05)。结论CaMKK2/AMPK/mTOR信号通路参与调控LIRI的炎症反应。Objective eTo investigate whether CaMKK2 alleviates lung ischemia reperfusion injury(LIRI)by regulating the AMPK pathway.Methods Forty-five 8-week-old healthy male C57BL/6 mice were evenly divided into sham group(Sham),lung ischemia-reperfusion group(IR group),and IR+CaMKK2 inhibitor group(CaMKK2 inhibitor group),15 per group.A mouse model of lung ischemia-reperfusion injury(LIRI)was established,and survival rate was evaluated by survival analysis,blood gas analysis was used to evaluate mouse respiratory function,lung wet dry weight ratio was used to evaluate pulmonary edema,HE staining was used to evaluate lung tissue pathology,and Western blot was used to analyze the expressions of NF-κ B,TNF-αand CaMKK2/AMPK/mTOR signaling pathway protein in lung tissue.Results Inhibition of CaMKK2 could increase mouse mortality caused by LIRI,exacerbate pulmonary edema and respiratory dysfunction(P<0.05),increase infiltration of inflammatory cells in lung tissue,and increase the expression of NF-κB and TNF-αin lung tissue,exacerbate the decrease in phosphorylated AMPK and the increase in phosphorylated mTOR(P<0.05).Conclusion The CaMKK2/AMPK/mTOR signaling pathway is involved in regulating the inflammatory response of LIRI.
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