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楤木皂苷抑制内毒素导致的心肌损伤和焦亡
引用本文:殷玥,陈迈,余璐.楤木皂苷抑制内毒素导致的心肌损伤和焦亡[J].心脏杂志,2019,31(6):643-647.
作者姓名:殷玥  陈迈  余璐
作者单位:1.基础医学院生理与病理生理学教研室 第四军医大学
基金项目:国家自然科学基金项目资助(31571413,81470410);陕西省社发攻关项目资助(2018SF-270)
摘    要: 目的 内毒素(LPS)导致的心功能障碍是脓毒血症患者死亡的重要原因。本研究旨在探讨采用楤木皂苷(saponins extracted from Aralia taibaiensis,sAT)能否抑制LPS导致的心肌损伤和心肌细胞焦亡。 方法 将雄性C57/BL6小鼠随机分为:正常对照组,sAT对照组,LPS组和LPS+sAT组,每组8只。采用sAT 240 mg/(kg·d),7天]灌胃后腹腔注射LPS (15 mg/kg),于24小时后检测心脏功能,同时测定各组炎症因子水平;Western blot检测caspase-11的表达。细胞学实验采用H9C2心肌细胞给予LPS结合常规焦亡刺激物—霍乱毒素B型亚单位(CTB)诱导心肌细胞焦亡,检测sAT对H9C2细胞存活率及细胞培养上清中IL-1β,LDH水平和细胞caspase-11水平的影响。 结果 与对照组相比,LPS导致心功能指标显著降低,血浆CK-MB显著升高,死亡率增高,心肌组织中炎症反应显著增强(P < 0.05)。给予sAT处理可显著改善LPS所导致的心功能障碍并抑制炎症反应,与LPS组相比,降低LPS组小鼠的死亡率(P < 0.05)。LPS可导致心肌组织出现细胞焦亡特征,表现为心肌caspase-11活化,IL-1β水平升高和血浆LDH水平显著升高;sAT处理可有效抑制LPS导致的心肌细胞焦亡。细胞学实验证实,LPS结合CTB可诱导H9C2心肌细胞焦亡,sAT处理可有效抑制细胞caspase-11活化,有效降低细胞培养上清中的IL-1β和LDH水平,显著提高细胞存活率。 结论 sAT能够抑制LPS导致的心肌损伤和心功能障碍,并有效抑制心肌细胞焦亡。

关 键 词:内毒素    心肌损伤    楤木皂苷    细胞焦亡
收稿时间:2019-04-09

Saponins extracted from Aralia Taibaiensis attenuates endotoxin-induced cardiac injury and pyroptosis
Institution:1.Department of physiology and pathophysiology, school of basic medicine2.Department of cardiovascular medicine, xijing hospital3.Department of Pathology, Xijing Hospital, Fourth Military Medical University, Xi’an 710032, Shaanxi, China
Abstract: AIM To investigate whether saponins extracted from Aralia taibaiensis (sAT) can inhibit myocardial damage and cardiomyocyte pyroptosis caused by endotoxin (LPS). METHODS Male C57/BL6 mice were randomly divided into normal control group, sAT control group, LPS group and LPS+sAT group, with 8 mice in each group. C57/BL6 mice were treated with sAT 240 mg/(kg·d) for 7 days], followed by intraperitoneal injection of LPS (15 mg/kg) for 24h. Cardiac functions and inflammatory factors were measured and cardiac caspase-11 was detected by Western blot. In cytology experiments, H9C2 cardiomyocytes were used to establish cell pyroptosis model induced by LPS combined with cholera toxin B-type subunit (CTB). The effect of sAT on the survival rate of H9C2 cells and the levels of IL-1β, LDH levels and caspase-11 was measured. RESULITS LPS caused significant cardiac dysfunction, increased plasma CK-MB level, significantly increased mortality and marked increased in inflammatory response in myocardial tissue compared with those in control group (P < 0.05). sAT treatment alleviated cardiac dysfunction, inhibited inflammatory response and decreased mortality in LPS group compared with those in LPS group (P < 0.05). LPS resulted in pyroptosis in myocardial tissue, which was characterized by myocardial caspase-11 activation, elevated IL-1β level and plasma LDH level. sAT treatment effectively inhibited myocardial pyroptosis caused by LPS. Cytological experiments confirmed that LPS combined with CTB induced the pyroptosis of H9C2 cardiomyocytes. sAT treatment effectively inhibited the activation of caspase-11, reduced the levels of IL-1β and LDH in cell culture supernatant, and significantly improved H9C2 cardiomyocytes survival rate. CONCLUSION sAT attenuates LPS induced myocardial injury and cardiac dysfunction and effectively inhibits myocardial pyroptosis.
Keywords:
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