BackgroundIntestinal mucosa barrier dysfunction after burn injury is an important factor for causing mortality of burn patients. The current study established a burn model in rats and used a free radical scavenger edaravone (ED) to treat the rats, so as to investigate the effect of edaravone on intestinal mucosa barrier after burn injury.MethodsAnesthetized rats were subjected to 40% total body surface area water burn immediately, followed by treatment with ED, scrambled antagomir, or antagomiR-320. Intestinal mucosa damage was observed by hematoxylin-eosin staining and graded by colon mucosal damage index (CMDI) score. The contents of total sulfhydryl (TSH), superoxide dismutase (SOD), catalase (CAT) and malondialdehyde (MDA) were determined by spectrophotometry. Cell apoptosis, protein relative expression,and the in situ expressions of p-Akt and p-Bad were detected by flow cytometry, Western blotting and immunohistochemistry, respectively. The miR-320 expression was determined by quantitative real-time polymerase chain reaction.ResultsED alleviated intestinal mucosal damage caused by burn injury, down-regulated the levels of MDA, cytochrome C, cleaved caspase-9 and cleaved caspase-3, but up-regulated the levels of TSH, SOD, CAT and Bcl-2. We also found that ED could reduce oxidative stress, inhibit cell apoptosis, increase the expressions of p-Akt, p-Bad and miR-320, and decrease PTEN expression. PTEN was predicted to be the target gene for miR-320, and cell apoptosis could be promoted by inhibiting miR-320 expression.ConclusionED regulates Akt/Bad/Caspase signaling cascade to reduce apoptosis and oxidative stress through up-regulating miR-320 expression and down-regulating PTEN expression, thus protecting the intestinal mucosal barrier of rats from burn injury.

中文翻译：

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依达拉奉通过上调 miR-320 表达减少烧伤后氧化应激和肠细胞凋亡

背景烧伤后肠黏膜屏障功能障碍是导致烧伤患者死亡的重要因素。本研究建立大鼠烧伤模型，并使用自由基清除剂依达拉奉(ED)治疗大鼠，以研究依达拉奉对烧伤后肠黏膜屏障的影响。方法麻醉大鼠全身40%立即用水烧伤区域，然后用 ED、炒 antagomir 或 antagomir-320 处理。通过苏木精-伊红染色观察肠黏膜损伤，并通过结肠黏膜损伤指数（CMDI）评分进行分级。分光光度法测定总巯基(TSH)、超氧化物歧化酶(SOD)、过氧化氢酶(CAT)和丙二醛(MDA)的含量。细胞凋亡、蛋白质相对表达、分别采用流式细胞术、Western blotting和免疫组化检测p-Akt和p-Bad的原位表达。通过实时定量聚合酶链反应测定miR-320的表达。结果ED减轻烧伤引起的肠黏膜损伤，下调MDA、细胞色素C、cleaved caspase-9和cleaved caspase-3的水平，但上调-调节 TSH、SOD、CAT 和 Bcl-2 的水平。我们还发现ED可以减轻氧化应激，抑制细胞凋亡，增加p-Akt、p-Bad和miR-320的表达，降低PTEN的表达。预测PTEN是miR-320的靶基因，抑制miR-320的表达可促进细胞凋亡。