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姜黄素对透明膜病(HMD)中促炎细胞因子表达的调节作用

Regulation of pro-inflammatory cytokine expression by curcumin in hyaline membrane disease (HMD).

作者信息

Literat A, Su F, Norwicki M, Durand M, Ramanathan R, Jones C A, Minoo P, Kwong K Y

机构信息

Department of Pediatrics, Women's and Children's Hospital, LAC+USC Medical Center, Los Angeles, CA 90033, USA.

出版信息

Life Sci. 2001 Dec 7;70(3):253-67. doi: 10.1016/s0024-3205(01)01398-4.

Abstract

Persistent expression of pro-inflammatory cytokines is believed to play a major role in the pathogenesis of chronic lung disease (CLD) in premature infants. Inhibition of pro-inflammatory cytokine production in the lungs of preterm newborns may result in the attenuation of CLD. Curcumin is a naturally occurring phenolic compound derived from the food spice tumeric with broad based in vitro anti-inflammatory properties. In this study lung inflammatory cells from preterm newborns at risk for the development of CLD were derived via modified broncho-alveolar lavage and stimulated ex vivo with lipopolysaccharide (LPS) (10 ng/ml). Curcumin was added to these cultures at 0, 0.5 and 20 uM concentrations. Pro-inflammatory cytokine, TNFalpha, IL-1beta and IL-8 protein was measured from the culture supernatants 12 hours post culture. For control, adult peripheral blood mononuclear cells (PBMC) were cultured under the same conditions. Both neonatal lung inflammatory cells and adult PBMC produced high levels of pro-inflammatory cytokines in response to LPS. Curcumin produced significant inhibition of IL-1beta and IL-8 but minimal inhibition of TNFalpha expression by preterm lung inflammatory cells at 20 uM concentrations. Adult PBMC expression of IL-8 was significantly inhibited by curcumin at 20 uM concentrations. Therefore, curcumin inhibits pro-inflammatory cytokine production (TNFalpha, IL-1beta and IL-8) by lung inflammatory cells ex vivo. Pathways involved with curcumin regulation of these cytokines are developmentally intact and functional in premature infants. Curcumin may be effective as a therapeutic agent in the attenuation of CLD.

摘要

促炎细胞因子的持续表达被认为在早产儿慢性肺病(CLD)的发病机制中起主要作用。抑制早产新生儿肺部促炎细胞因子的产生可能会减轻CLD。姜黄素是一种天然存在的酚类化合物,源自食品香料姜黄,具有广泛的体外抗炎特性。在本研究中,通过改良的支气管肺泡灌洗从有CLD发生风险的早产新生儿中获取肺部炎性细胞,并在体外用脂多糖(LPS)(10 ng/ml)进行刺激。将姜黄素以0、0.5和20 μM的浓度添加到这些培养物中。培养12小时后,从培养上清液中测量促炎细胞因子TNFα、IL-1β和IL-8蛋白。作为对照,成年外周血单核细胞(PBMC)在相同条件下培养。新生儿肺部炎性细胞和成年PBMC对LPS均产生高水平的促炎细胞因子。在20 μM浓度下,姜黄素对早产肺部炎性细胞的IL-1β和IL-8产生显著抑制,但对TNFα表达的抑制作用最小。在20 μM浓度下,姜黄素对成年PBMC的IL-8表达有显著抑制作用。因此,姜黄素在体外可抑制肺部炎性细胞产生促炎细胞因子(TNFα、IL-1β和IL-8)。姜黄素对这些细胞因子的调节途径在早产儿中发育完整且具有功能。姜黄素可能作为一种治疗剂有效减轻CLD。

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