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首页> 外文期刊>The Korean Journal of Physiology & Pharmacology >Inhibition of Inducible Nitric Oxide Synthase Attenuates Monosodium Urate-induced Inflammation in Mice
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Inhibition of Inducible Nitric Oxide Synthase Attenuates Monosodium Urate-induced Inflammation in Mice

机译：诱导型一氧化氮合酶的抑制作用减弱尿酸一钠诱导的小鼠炎症。

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摘要

The present study elucidated the effect of the selective inducible nitric oxide synthase (iNOS) inhibitor N6-(1-iminoethyl)-L-lysine (L-NIL) on monosodium urate (MSU) crystal-induced inflammation and edema in mice feet. L-NIL (5 or 10 mg/kg/day) was administered intraperitoneally 4 h before injection of MSU (4 mg) into the soles of mice hindlimb feet. Twenty-four hours after MSU injection, foot thickness was increased by 160% and L-NIL pretreatment reduced food pad swelling in a dose dependent manner. Pretreatment of 10 mg/kg/day L-NIL significantly suppressed the foot pad swelling by MSU. Plasma level of nitric oxide (NO) metabolites and gene expression and protein level of iNOS in feet were increased by MSU, which was suppressed by L-NIL pretreatment. Similar pattern of change was observed in nitrotyrosine level. MSU increased the gene expression of tumor necrosis factor (TNF)-α and interleukin (IL)-1β and L-NIL pretreatment suppressed MSU-induced cytokines expression. The mRNA levels of superoxide dismutase and glutathione peroxidase1 were increased by MSU and L-NIL pretreatment normalized the gene expression. Phosphorylation of extracellular signal-regulated kinase 1/2 and p38 was increased by MSU, which was suppressed by L-NIL pretreatment. The mRNA levels of iNOS, TNF-α, and IL-1β were increased by MSU in human dermal fibroblasts, C2C12 myoblasts, and human fetal osteoblasts in vitro , which was attenuated by L-NIL in a dose dependent manner. This study shows that L-NIL inhibits MSU-induced inflammation and edema in mice feet suggesting that iNOS might be involved in MSU-induced inflammation.
机译：本研究阐明了选择性诱导型一氧化氮合酶（iNOS）抑制剂N 6 -（1-亚氨基乙基）-L-赖氨酸（L-NIL）对尿酸钠（MSU）晶体诱导的影响小鼠脚发炎和水肿。在将MSU（4 mg）注入小鼠后肢足底之前4 h腹膜内给予L-NIL（5或10 mg / kg / day）。 MSU注射后二十四小时，脚的厚度增加了160％，L-NIL预处理以剂量依赖的方式减少了食物垫肿胀。 L-NIL 10 mg / kg / day的预处理可显着抑制MSU引起的足垫肿胀。 MSU增加了脚中一氧化氮（NO）代谢物的血浆水平以及iNOS的基因表达和蛋白质水平，而L-NIL预处理抑制了血浆中iNOS的基因表达和蛋白质水平。硝基酪氨酸水平也观察到类似的变化模式。 MSU增加了肿瘤坏死因子（TNF）-α和白介素（IL）-1β的基因表达，L-NIL预处理抑制了MSU诱导的细胞因子表达。 MSU增加了超氧化物歧化酶和谷胱甘肽过氧化物酶1的mRNA水平，L-NIL预处理使基因表达正常化。 MSU增强了细胞外信号调节激酶1/2和p38的磷酸化，而L-NIL预处理抑制了磷酸化。 MSU在体外使人皮肤成纤维细胞，C2C12成肌细胞和人胎儿成骨细胞中的iNOS，TNF-α和IL-1β的mRNA水平升高，并被L-NIL减弱，呈剂量依赖性。这项研究表明，L-NIL抑制了MSU诱发的小鼠足部炎症和水肿，表明iNOS可能参与了MSU诱发的炎症。

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