Effects of ketamine and propofol on inflammatory responses of primary glial cell cultures stimulated with lipopolysaccharide
Effects of ketamine and propofol on inflammatory responses of primary glial cell cultures stimulated with lipopolysaccharide
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DOI：
10.1093/bja/aei256
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发表时间：
2005-12-01
影响因子：
9.8
通讯作者：
Andoh, T
中科院分区：
文献类型：
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作者：
Shibakawa, YS;Sasaki, Y;Andoh, T
背景。据报道，氯胺酮在体外和体内对脂多糖（LPS）刺激的巨噬细胞具有抗炎作用。几项研究报告了关于异丙酚对免疫细胞产生细胞因子的影响的相互矛盾的结果。然而，目前还没有关于这些药物对神经胶质细胞炎症反应影响的报道。我们研究了氯胺酮和丙泊酚对 LPS 诱导的大鼠神经胶质细胞体外原代培养物中一氧化氮、肿瘤坏死因子-α (TNF-α) 和前列腺素 E-2 (PGE(2)) 产生的影响。方法。在存在和不存在不同浓度的氯胺酮（30-1000μM）或丙泊酚（30和300μM）的情况下用LPS刺激神经胶质细胞。通过使用 Griess 反应测量亚硝酸盐来确定释放到培养基中的一氧化氮，并通过酶联免疫吸附测定 (ELISA) 测量 TNF-α 和 PGE(2) 的浓度。 结果。在混合神经胶质细胞、星形胶质细胞培养物和小胶质细胞培养物中，氯胺酮减少 LPS 诱导的 TNF-α 产生，但不显着抑制亚硝酸盐释放。氯胺酮还可以抑制星形胶质细胞培养物中 LPS 诱导的 PGE(2) 产生。相反，异丙酚对混合胶质细胞中 LPS 诱导的亚硝酸盐或 TNF-α 的产生没有影响。结论。数据表明，氯胺酮抑制了用 LPS 处理的星形胶质细胞和小胶质细胞的一些炎症反应，而不会引起一氧化氮释放的重大变化。异丙酚对 LPS 刺激的神经胶质细胞产生一氧化氮或 TNF-α 没有影响。
Background. Ketamine has been reported to exert anti-inflammatory effects on macrophages stimulated with lipopolysaccharide (LPS) in vitro and in vivo. Several studies have reported conflicting results regarding the effects of propofol on cytokine production from immune cells. However, there have been no reports of the effects of these agents on inflammatory responses in glial cells. We investigated the effects of ketamine and propofol on LPS-induced production of nitric oxide, tumour necrosis factor-alpha (TNF-alpha) and prostaglandin E-2 (PGE(2)) from primary cultures of rat glial cells in vitro.Methods. Glial cells were stimulated with LPS in the absence and presence of various concentrations of ketamine (30-1000 mu M) or propofol (30 and 300 mu M). Nitric oxide released into the culture media was determined by measuring nitrite using the Griess reaction, and concentrations of TNF-alpha and PGE(2) were measured by enzyme-linked immunosorbent assay (ELISA).Results. Ketamine reduced LPS-induced TNF-alpha production without significant inhibition of nitrite release in mixed glial cells, astrocyte cultures and microglial cultures. Ketamine also inhibited LPS-induced production of PGE(2) in astrocyte cultures. In contrast, propofol had no effect on LPS-induced nitrite or TNF-alpha production in mixed glial cells.Conclusions. The data demonstrate that ketamine inhibited some of the inflammatory responses of both astrocytes and microglial cells treated with LPS without causing major change in nitric oxide release. Propofol had no effect on the production of nitric oxide or TNF-alpha from LPS-stimulated glial cells.