Essential nutrients suppress inflammation by modulating key inflammatory gene expression
Essential nutrients suppress inflammation by modulating key inflammatory gene expression
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DOI：
10.3892/ijmm_00000079
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发表时间：
2008-12-01
影响因子：
5.4
通讯作者：
Niedzwiecki, A.
中科院分区：
文献类型：
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作者：
Ivanov, V.;Cha, J.;Niedzwiecki, A.
我们研究了由抗坏血酸、槲皮素、柚皮素、橙皮素组成的营养混合物（NM）的文件效应。茶儿茶素赖氨酸、脯氨酸、精氨酸和N-乙酰半胱氨酸对细菌脂多糖（LPS）引发的实验性体内和体外炎症的影响。给BALB/c小鼠（n=36）施用NM（200 mg/kg BW）或布洛芬（20 mg/kg，BW）两周。血浆，在单次腹膜内注射LPS（lmg/kg BW）后三小时收集。用14种细胞因子芯片进行分析。通过细胞因子释放在人U937巨噬细胞中分析LPS炎症作用。环氧合酶（考克斯）酶活性、考克斯蛋白表达（Western印迹分析）。特异性mRNA水平（RT-PCR）和核因子κ β（NF κ β）活化（磷酸化p65免疫测定）。小鼠中的营养补充以与布洛芬类似的方式改变了LPS诱导的细胞因子应答（r=0.4157）。p=0.139）。在培养的巨噬细胞中对LPS的细胞因子应答与体内研究相似（r=0.718 p=0.023）。NM抑制考克斯-2酶活性，并且NM在转录水平c下调考克斯-2和促炎细胞因子蛋白表达水平，补充NF κ β激活的阻断。NM通过靶向参与对病原体的炎症反应的复杂过程中的多种负责机制，对实验性炎症表现出强烈的有益作用。
We investigated file effects of a nutrient mixture (NM) consisting of ascorbic acid, quercetin, naringenin, hesperetin. tea catechins. lysine, proline, arginine and N-acetyl cysteine on experimental in vivo and in vitro inflammation triggered by bacterial lipopolysaccharide (LPS). BALB/c mice (n=36) were administered NM (200 mg/kg BW) or ibuprofen (20 mg/kg, BW) for two weeks. Blood plasma, collected three hours after a single intraperitoneal injection with LPS (1 mg/kg BW). was analyzed with 14 cytokine microarray. LPS inflammatory effects were analyzed in human U937 macrophages by cytokine release. cyclooxygenase (COX) enzymatic activity, COX protein expression (Western blot analysis). specific mRNA levels (RT-PCR), and nuclear factor kappa beta (NF kappa beta) activation (phosphorylated p65 immunoassay). Nutrient Supplementation in mice altered the LPS-induced cytokine response in a manner similar to ibuprofen (r=0.4157. p=0.139). Cytokine response to LPS ill Cultured macrophages was similar to the in vivo Study (r=0.718 p=0.023). NM inhibited COX-2 enzymatic activity, and COX-2 and pro-inflammatory cytokine protein expression levels were downregulated by NM at the transcription level c complementing a blockade in NF kappa beta activation. NM demonstrated strong beneficial effects oil the experimental inflammation by targeting multiple responsible mechanisms in the complex process involved in the inflammatory reaction to pathogens.