中国学者再获美国肠外肠内营养学会临床营养周优秀奖
美国肠外肠内营养学会（ASPEN）第40届临床营养周（CNW）将于2017年2月18～21日在美国佛罗里达首府奥兰多召开。
2017年1月31日，ASPEN官方期刊《肠外肠内营养杂志》正式发表第40届CNW获奖研究论文摘要共41篇，包括瓦尔奖提名5篇、学员奖3篇、专题最佳奖6篇、国际奖11篇、优秀奖33篇。
其中，中国重庆新桥医院（第三军医大学第二附属医院）李良子、于敏、肖卫东、杨桦的《芳香烃受体对小鼠结肠炎的缓解作用及机制研究》被评选为重症专题国际优秀海报摘要。
该研究探讨了芳香烃受体（AhR）及其激动剂吲哚并[3,2-B]咔唑-6-甲醛（FICZ）对葡聚糖硫酸钠（DSS）诱导的小鼠结肠炎的缓解作用及其机制。
该研究将成年雄性C57BL/6小鼠随机分为正常对照组、DSS组（每天给予DSS喂养，连续7d）、DSS＋FICZ组（给予DSS喂养连续7d，从第3天开始腹腔注射1mg芳香烃受体激动剂FICZ）。每天检测小鼠体重变化，7d后HE染色观察结肠病理学变化，qPCR检测小鼠结肠上皮细胞炎性因子的表达。
结果发现，与正常对照组相比，模型组中小鼠体重明显减轻（P＜0.05），结肠长度缩短，肠黏膜明显损伤，促炎因子IL-1β、IL-6和肿瘤坏死因子（TNF）-α的表达升高（P＜0.05），保护性的细胞因子IL-10的表达变化不明显；与模型组相比，实验组中小鼠体重下降明显减少（P＜0.05），结肠长度增加，肠黏膜损伤减轻，同时促炎因子IL-1β、IL-6、TNF-α的表达降低（P＜0.05），保护性细胞因子IL-10明显升高（P＜0.05）。
因此，芳香烃受体（AhR）对小鼠结肠炎具有抑制作用，可能是通过下调促炎因子IL-1β、IL-6和TNF-α的表达，上调抗炎因子IL-10的表达发挥作用。
JPEN J Parenter Enteral Nutr. 2017;41(2):289.
Aryl Hydrocarbon Receptor Activation Ameliorate DSS-Induced Colitis Through Up-Regulate the Expression of IEC-Derived IL-10.
Liangzi Li, Min Yu, Weidong Xiao, Hua Yang.
General Surgery, Xinqiao Hospital, Chongqing, China.
PURPOSE: The aryl hydrocarbon receptor (AhR) is a cytoplasmic transcription factor activated by a large variety of environmental agents. Activation of the AhR is involved in the control of intestinal mucosal homeostasis and thought to suppress inflammatory bowel disease (IBD). Interleukin-10 (IL-10) is proved to be an important anti-inflammatory cytokine that ameliorates mucosal inflammation. The goal of this study was to investigate the role of AhR activation in alleviating intestinal inflammation by upregulating IL-10 in intestinal epithelial cells (IECs).
METHODS: Adult C57BL/6 mice were treated with 3.5% dextran sulfate sodium (DSS) for 7 days. The mice were given injections of the AhR ligand 6-formylindolo (3,2-b) carbazole (FICZ) starting 2 days after the first administration of DSS. Mice were weighted, colon tissues were collected and measured, and histology analyses were performed. IECs were isolated from colon, and the expression of IL-10 in IECs was assessed by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot analysis. Caco-2 intestinal epithelial cells were treated with lipopolysaccharide (LPS) for 24 hours, with or without FICZ, and IL-10 expression was detected by Western blot analysis and qRT-PCR. Additionally, Caco-2 cells were treated with AhR siRNA, and expression of IL-10 was studied with Western blot analysis and qRT-PCR.
RESULTS: Administration of FICZ to mice with DSS-induced colitis resulted a significant increase in AhR expression detected by Western blot analysis and qRT-PCR. Histological examination of colonic tissues showed that more injury was observed in the DSS group than in the FICZ + DSS group. Furthermore, administration of FICZ greatly decelerated the weight loss induced by DSS. Western blot analysis and qRT-PCR showed FICZ significantly increased the expression of IEC-derived IL-10 both in the colons of mice with DSS-induced colitis and LPS-treated Caco-2 cells. FICZ also increased the expression of phosphorylated STAT3 in LPS-treated Caco-2 cells. Interestingly, inhibition of STAT3 phosphorylation by Stattic counteracted FICZ-induced increase of IL-10 expression in Caco-2 cells.
CONCLUSIONS: FICZ-induced AhR activation could upregulate the expression of IEC-derived IL-10 and ameliorate DSS-induced colitis. AhR-related compounds might be the potential therapeutic methods for the treatment of patients with IBD.
FINANCIAL SUPPORT: None.
DOI: 10.1177/0148607116686023
CLINICAL NUTRITION WEEK 2017: Orlando, Florida, February 18-21, 2017.
AWARDED ABSTRACTS: Vars Candidates, Trainee Awards, Best of CNW (Topic Awards), International Awards, and Abstracts of Distinction.
The Harry M. Vars award is given annually to the person presenting the highest-scoring qualified abstract for Clinical Nutrition Week (CNW). The candidates are also evaluated on a manuscript based on their abstract, as well as on their expertise and knowledge of the science as demonstrated during their oral presentation at the Premier Paper Session. CNW17 is February 18-21 in Orlando, Florida.
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