Monitoring of inflammatory mediators induced by silk sericin
Monitoring of inflammatory mediators induced by silk sericin
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DOI：
10.1016/j.jbiosc.2008.12.012
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发表时间：
2009-05-01
影响因子：
2.8
通讯作者：
Srichana, Teerapol
中科院分区：
文献类型：
--
作者：
Aramwit, Pornanong;Kanokpanont, Sorada;Srichana, Teerapol
蚕丝蛋白已被证明是生物医学材料的良好候选者。然而，已经有一些关于蚕丝丝胶蛋白的免疫和过敏反应的报道。我们的目的是研究在体外和体内由丝胶蛋白诱导的炎症介质。小鼠单核细胞和肺泡巨噬细胞系用于监测由浓度为0.2-1.0 mg/mL的丝胶蛋白激活后产生的白细胞介素（IL）-1 β和肿瘤坏死因子（TNF）-α的水平。两种细胞系产生的TNF-α和IL-1 β的量以剂量依赖性方式与培养基中的丝胶蛋白浓度相对应。在由巨噬细胞活化的丝胶蛋白后产生的TNF-α和IL-1 β的水平高于由单核细胞产生的水平。然而，这些细胞因子水平不会级联其他炎症反应。还监测了来自经丝氨酸处理的、经乳膏基质处理的和正常盐水浸泡的全层大鼠切除物的炎症介质。使用伤口尺寸测量和ELISA测定，与乳膏基质处理和正常盐水浸泡的伤口相比，经丝氨酸处理的伤口愈合更快，并且具有更低水平的炎症介质。可以得出结论，丝胶蛋白促进伤口愈合过程而不引起炎症。(c)2008年，日本生物技术学会。All rights reserved.
Silk proteins have been shown to be good candidates for biomedical materials. However, there have been some reports regarding immunological and allergic responses to silk sericin. Our objective was to investigate the inflammatory mediators induced by sericin both in vitro and in vivo. Mouse monocyte and alveolar macrophage cell lines were used for monitoring levels of interleukin (IL)-1 beta and tumor necrosis factor (TNF)-alpha generated after activation by sericin at concentrations of 0.2-1.0 mg/mL The amounts of TNF-alpha and IL-1 beta produced by both cell lines corresponded, in a dose-dependent manner, with the sericin concentration in the culture medium. The levels of TNF-alpha and IL-1 beta generated after sericin activation by macrophage cells were higher than those generated by monocytes. However, these cytokine levels would not cascade to other inflammatory effects. Inflammatory mediators were also monitored from sericin-treated, cream base-treated and normal saline-soaked full-thickness rat excisions. Using wound size measurements and ELISA assays, sericin-treated wounds were shown to heal faster and had lower levels of inflammatory mediators, as compared with the cream base-treated and normal saline-soaked wounds. It can be concluded that sericin promotes the wound healing process without causing inflammation. (c) 2008, The Society for Biotechnology, Japan. All rights reserved.