异丙酚对人羊膜源性WISH细胞脂多糖诱导的炎症反应具有保护作用。

Cheul-Hong Kim, Sang-Hoon Lee, Ji-Young Yoon, Eun-Jung Kim, Jong Hoon Joo, Yeon Ha Kim, Eun-Ji Choi
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引用次数: 0

摘要

背景:妊娠期间有时需要非产科手术,孕妇颈部脓肿或面部骨折手术不能推迟。然而,牙科手术可能会有压力,并可能引起炎症,而炎症反应是众所周知的早产的主要原因。异丙酚是一种静脉麻醉药,通常用于全身麻醉和镇静。关于异丙酚对人羊膜影响的研究很少。本研究研究了异丙酚对人羊膜源性WISH细胞中脂多糖(LPS)诱导的炎症反应的影响。方法:将WISH细胞暴露于LPS 24 h后,与不同浓度异丙酚(0.01-1µg/ml)共处理。采用MTT法测定细胞活力。采用基于Griess反应的微量测定法分析了一氧化氮(NO)的产生。western blotting分析环氧化酶-2 (COX-2)、前列腺素E2 (pge2)、p38、phospho-p38蛋白的表达。结果:异丙酚不影响许愿细胞的活力和NO的产生。LPS和异丙酚共处理可降低WISH细胞中COX-2和PGE2蛋白的表达,抑制p38磷酸化。结论:异丙酚不影响WISH细胞活力,抑制lps诱导的炎症因子表达。异丙酚对炎症因子表达的抑制作用可能是通过抑制p38激活介导的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Propofol protects against lipopolysaccharide-induced inflammatory response in human amnion-derived WISH cells.

Propofol protects against lipopolysaccharide-induced inflammatory response in human amnion-derived WISH cells.

Propofol protects against lipopolysaccharide-induced inflammatory response in human amnion-derived WISH cells.

Propofol protects against lipopolysaccharide-induced inflammatory response in human amnion-derived WISH cells.

Background: Nonobstetric surgery is sometimes required during pregnancy, and neck abscess or facial bone fracture surgery cannot be postponed in pregnant women. However, dental surgery can be stressful and can cause inflammation, and the inflammatory response is a well-known major cause of preterm labor. Propofol is an intravenous anesthetic commonly used for general anesthesia and sedation. Studies investigating the effect of propofol on human amnion are rare. The current study investigated the effects of propofol on lipopolysaccharide (LPS)-induced inflammatory responses in human amnion-derived WISH cells.

Methods: WISH cells were exposed to LPS for 24 h and co-treated with various concentrations of propofol (0.01-1 µg/ml). Cell viability was measured using the MTT assay. Nitric oxide (NO) production was analyzed using a microassay based on the Griess reaction. The protein expression of cyclooxygenase-2 (COX-2), prostaglandin E2 (PGE 2), p38, and phospho-p38 was analyzed using western blotting.

Results: Propofol did not affect the viability and NO production of WISH cells. Co-treatment with LPS and propofol reduced COX-2 and PGE2 protein expression and inhibited p38 phosphorylation in WISH cells.

Conclusion: Propofol does not affect the viability of WISH cells and inhibits LPS-induced expression of inflammatory factors. The inhibitory effect of propofol on inflammatory factor expression is likely mediated by the inhibition of p38 activation.

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