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作 者:胡云芝[1] 李军民[2] 鲁之中[2] 李卫[2] 姜富国 桂静 HU Yunzhi;LI Junmin;LU Zhizhong;LI Wei;JIANG Fuguo;GUI Jing(Department of Pediatrics,Jiaozuo People's Hospital,Jiaozuo 454002,China;Department of Clinical Laboratory,Jiaozuo People’s Hospital,Jiaozuo 454002,China)
机构地区:[1]河南省焦作市人民医院儿科,454002 [2]河南省焦作市人民医院检验科,454002
出 处:《免疫学杂志》2020年第2期132-137,共6页Immunological Journal
基 金:北京市医学科学研究基金(YWJKJJHKYJJ-B17817)
摘 要:目的探究白茅苷(imperatorin,Imp)对缺氧缺血性脑损伤模型新生大鼠心肌损伤和免疫反应的影响及作用机制。方法将大鼠随机分为:假手术组(Ctrl组)、模型组(MCAO组)、MCAO+Imp(2.5、5、10 mg)组,MCAO法诱导缺氧缺血性脑损伤新生大鼠模型。检测心肌组织病理学改变,增殖、凋亡相关蛋白表达,心肌损伤和炎症因子含量,及信号通路表达。结果白茅苷能改善MCAO新生大鼠心肌组织病理损伤,上调心肌组织Ki67、PCNA表达(P<0.01),上调Bcl-2、下调Bax、Caspase-3和Caspase9表达(P<0.01),降低Mb、cTnI和CK-MB血清含量(P<0.01),减少IL-1β、iNOS和IL-6,增加IL-10含量(P<0.01),同时下调TGF-β1、P-P65/P65和TNF-α表达水平(P<0.01)。结论白茅苷能减轻缺氧缺血性脑损伤模型新生大鼠的心肌损伤,并抑制免疫反应,其机制与抑制TGF-β1/NF-κB p65/TNF-α炎症通路活化相关。This study was performed to explore the effects of imperatorin(Imp)on myocardial injury and immune response in neonatal rats with hypoxic-ischemic brain injury.Rats were randomly divided into sham operation group(Ctrl group),model group(MCAO group),MCAO+Imp(2.5,5,10 mg)groups.The neonatal rat model of hypoxic-ischemic brain injury were induced with MCAO method.Corresponding methods were used to detect the pathological changes of myocardium,the expression of proliferation and apoptosis-related proteins,the myocardial injury and inflammatory factors levels,and the expression of signaling pathways.Data showed that Imp could ameliorate the myocardial pathological injury in MCAO neonatal rats,increase the expression of Ki67 and PCNA in myocardial tissue(P<0.01),up-regulate the expression levels of Bcl-2(P<0.01),down-regulate Bax,Caspase-3 and Caspase-9(P<0.01),decrease the contents of Mb,cTnI,CK-MB,IL-1β,NOS and IL-6,increase the level of IL-10(P<0.01),while down-regulate the expression of TGF-β1,P-P65/P65 and TNF-αproteins(P<0.01).In conclusion,imperatorin can alleviate myocardial injury and inhibit immune responses in neonatal rats with hypoxicischemic brain injury,and the mechanism is related to inhibiting the activation of TGF-β1/NF-κB p65/TNF-αinflammatory pathway.
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