Anti-inflammatory activity of a globular adiponectin function on RAW 264 cells stimulated by lipopolysaccharide from Aggregatibacter actinomycetemcomitans
Anti-inflammatory activity of a globular adiponectin function on RAW 264 cells stimulated by lipopolysaccharide from Aggregatibacter actinomycetemcomitans
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DOI：
10.1111/j.1574-695x.2009.00573.x
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发表时间：
2009-08-01
影响因子：
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通讯作者：
Yamashita, Yoshihisa
中科院分区：
文献类型：
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作者：
Kamio, Noriaki;Akifusa, Sumio;Yamashita, Yoshihisa
脂联素是一种具有抗炎作用的脂肪因子。我们以前报道过，球状脂联素（gAd）抑制伴放线杆菌脂多糖诱导的核因子-κ B活性，这表明gAd的抗炎作用。在本研究中，我们研究了gAd是否能够调节A.在小鼠巨噬细胞系（RAW 264）中，放线菌伴放线菌脂多糖对细胞因子诱导的影响。A. p38丝裂原活化蛋白激酶、c-Jun N-末端激酶、细胞外信号调节激酶和I κ B激酶α/β的磷酸化和I κ B的降解。与未处理的细胞相比，在gAd预处理的RAW 264细胞中，伴随放线菌脂多糖中毒明显减少。通过实时PCR评估肿瘤坏死因子（TNF）-α和白细胞介素-10（IL-10）mRNA的表达水平。刺激12小时后收集无细胞上清液，并通过酶联免疫吸附测定法分析TNF-α和IL-10。gAd预处理对A.伴放线菌脂多糖诱导的TNF-α mRNA表达和蛋白分泌。与此相反，gAd预处理显著增强A.伴放线菌脂多糖诱导IL-10 mRNA表达和蛋白分泌。这些数据表明了gAd在局部炎性病变（如牙周炎）中的抗炎活性机制。
Adiponectin is an adipokine with potent anti-inflammatory properties. We previously reported that a globular adiponectin (gAd) suppresses Aggregatibacter actinomycetemcomitans lipopolysaccharide-induced nuclear factor-kappa B activity, suggesting an anti-inflammatory effect of gAd. In this study, we investigated whether gAd is able to modulate the effect of A. actinomycetemcomitans lipopolysaccharide on cytokine induction in a murine macrophage cell line (RAW 264). The phosphorylation of p38 mitogen-activated protein kinase, c-Jun N-terminal kinase, extracellular signal-regulated kinase, and I kappa B kinase alpha/beta and the degradation of I kappa B, which were induced by A. actinomycetemcomitans lipopolysaccharide intoxication, were clearly reduced in gAd-pretreated RAW 264 cells compared with the untreated cells. Expression levels of tumor necrosis factor (TNF)-alpha and interleukin-10 (IL-10) mRNA were assessed by real-time PCR. Cell-free supernatants were collected after 12 h of stimulation and analyzed by enzyme-linked immunosorbent assay for TNF-alpha and IL-10. Pretreatment with gAd significantly inhibited the A. actinomycetemcomitans lipopolysaccharide-induced TNF-alpha mRNA expression and protein secretion. In contrast, pretreatment with gAd significantly enhanced the A. actinomycetemcomitans lipopolysaccharide-induced IL-10 mRNA expression and protein secretion. These data suggest a mechanism for the anti-inflammatory activity of gAd in local inflammatory lesions, such as periodontitis.