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作 者:曾海平 吴东方[2] 胡云双 ZENG Haiping;WU Dongfang;HU Yunshuang(Department of Laboratory Medicine,Wenzhou Hospital of Integrated Traditional Chinese and Western Medicine,Wenzhou 325000,China;School of Laboratory Medicine and Life Science,Wenzhou Medical University,Whenzou 325035,China)
机构地区:[1]温州市中西医结合医院检验科,浙江温州325000 [2]温州医科大学检验医学院生命科学学院,浙江温州325035
出 处:《温州医科大学学报》2021年第9期746-750,754,共6页Journal of Wenzhou Medical University
摘 要:目的:研究紫檀芪(PTS)对脓毒症致大鼠膈肌损伤的作用及其可能机制。方法:通过盲肠结扎穿刺术建立大鼠脓毒症模型。将大鼠随机分为3组:假手术组、脓毒症组和PTS组(25 mg/kg),24 h后处死大鼠,采集膈肌进行组织病理学检查及膈肌损伤评分(DDS);TUNEL染色法检测膈肌组织细胞凋亡;ELISA法测定膈肌组织中IL-1β、TNF-α、IL-6、AST、LDH、CK及MPO含量;Western blot检测膈肌组织中p-PI3K和p-Akt的表达。结果:与假手术组相比较,脓毒症组中DDS评分、细胞凋亡率、IL-1β、TNF-α、IL-6、AST、LDH、CK及MPO含量均明显升高,而p-PI3K和p-Akt蛋白含量下调,差异有统计学意义(P<0.05)。相比脓毒症组,PTS组中DDS评分、细胞凋亡率、IL-1β、TNF-α、IL-6、AST、LDH、CK及MPO含量均明显下调,而p-PI3K和p-Akt蛋白含量上调,差异有统计学意义(P<0.05)。结论:PTS通过PI3K/Akt途径抑制脓毒症致大鼠膈肌损伤。Objective:To explore the protective effect of pterostilbene(PTS)on sepsis-induced diaphragm injury and its possible mechanism in a rat model.Methods:Sepsis model was induced by cecal ligation and puncture(CLP)in rats.The rats,randomly divided into three groups:sham group,CLP group and PTS groups(25 mg/kg),were killed after CLP for 24 h.Diaphragm tissues were collected for pathological analysis and diaphragm Damage Score(DDS)detection.The apoptosis of diaphragm tissues was evaluated using TUNEL assay.The content of IL-1β,TNF-α,IL-6,AST,LDH,CK and MPO in diaphragm specimen was measured by ELISA assay.Western blot was used to explore the level of p-Akt and p-PI3K in diaphragm tissues.Results:Compared with sham group,the DDS score,apoptotic rate and the content of IL-1β,TNF-α,IL-6,AST,LDH,CK and MPO in CLP group were all promoted markedly.The level of p-Akt and p-PI3K was reduced during sepsis.However,the DDS score,apoptotic rate and the content of IL-1β,TNF-α,IL-6,AST,LDH,CK and MPO in CLP group were all markedly decreased by the administration of PTS,while the expression of p-Akt and p-PI3K was both increased after PTS treatment.Conclusion:PTS plays a protective role in diaphragm via PI3K/Akt pathway in a CLP-induced sepsis rat model,which provides a candidate for drug therapy of sepsis-induced diaphragm injury.
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