Posttreatment with dexmedetomidine aggravates LPS-induced myocardial dysfunction partly via activating cardiac endothelial α2A-AR in mice

Xiangxu Tang,Chanjuan Zhang,Tian Tian,Xiaomeng Dai,Yun Xing,Yingwei Wang,Duomeng Yang,Hongmei Li,Yiyang Wang,Xiuxiu Lv,Huadong Wang

International Immunopharmacology（2023）

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摘要

•Dexmedetomidine (DEX) posttreatment reduced survival in septic mice via α2A- AR.•DEX posttreatment aggravated LPS-induced cardiomyopathy by activating α2A- AR.•DEX posttreatment enhanced LPS-induced cardiac endothelial activation via α2A-AR.•DEX posttreatment promoted p38 pathway via PKC in LPS-treated cardiac endothelium.

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关键词

Sepsis,Myocardial dysfunction,Dexmedetomidine,α2A adrenergic receptor,Cardiac endothelial cells

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