Propofol inhibits lipopolysaccharide-induced tumor necrosis factor-alpha expression and myocardial depression through decreasing the generation of superoxide anion in cardiomyocytes.
Propofol inhibits lipopolysaccharide-induced tumor necrosis factor-alpha expression and myocardial depression through decreasing the generation of superoxide anion in cardiomyocytes.
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丙泊酚通过减少心肌细胞中超氧阴离子的产生来抑制脂多糖诱导的肿瘤坏死因子-α 表达和心肌抑制。
DOI：
10.1155/2014/157376
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发表时间：
2014
影响因子：
--
通讯作者：
Qin ZS
中科院分区：
文献类型：
--
作者：
Tang J;Hu JJ;Lu CH;Liang JN;Xiao JF;Liu YT;Lin CS;Qin ZS
TNF-α已被证明是脓毒症中心肌抑制的主要因素。本研究的目的是研究麻醉剂异丙酚对体内和体外LPS处理心肌细胞中TNF-α表达的影响。在培养的心肌细胞中，与对照组相比，异丙酚显著降低了gp91phox的蛋白表达和细胞外调节蛋白激酶1/2 （ERK1/2）和p38 MAPK的磷酸化，这与TNF-α的产生减少有关。在小鼠体内研究中，异丙酚可显著改善LPS处理后或内毒素血症小鼠的心肌抑制和提高存活率，这与心肌TNF-α生成、gp91phox、ERK1/2和p38 MAPK减少有关。由此可见，异丙酚可通过gp91phox/ERK1/2或p38 MAPK信号通路，消除lps诱导的TNF-α产生，缓解心脏抑制。本研究结果对应用异丙酚治疗脓毒症具有重要的临床意义。
TNF-α has been shown to be a major factor responsible for myocardial depression in sepsis. The aim of this study was to investigate the effect of an anesthetic, propofol, on TNF-α expression in cardiomyocytes treated with LPS both in vivo and in vitro. In cultured cardiomyocytes, compared with control group, propofol significantly reduced protein expression of gp91phox and phosphorylation of extracellular regulated protein kinases 1/2 (ERK1/2) and p38 MAPK, which associates with reduced TNF-α production. In in vivo mice studies, propofol significantly improved myocardial depression and increased survival rate of mice after LPS treatment or during endotoxemia, which associates with reduced myocardial TNF-α production, gp91phox, ERK1/2, and p38 MAPK. It is concluded that propofol abrogates LPS-induced TNF-α production and alleviates cardiac depression through gp91phox/ERK1/2 or p38 MAPK signal pathway. These findings have great clinical importance in the application of propofol for patients enduring sepsis.
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影响因子：
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作者：
Wang H;Wang G;Wang C;Wei Y;Wen Z;Wang C;Zhu A
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37.8
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DOI：
10.1186/cc7963
发表时间：
2009
期刊：
Critical care (London, England)
影响因子：
--
作者：
Barkhausen T;Hildebrand F;Krettek C;van Griensven M
通讯作者：
van Griensven M