摘要： 目的观察核因子κB （NF-κB）调控自噬在高脂饮食下葡聚糖硫酸钠（DSS）诱导的小鼠溃疡性结肠炎中的作用及其机制。方法将小鼠分为正常对照组（Control组）、高脂饮食组（HFD组）、DSS组、DSS+高脂饮食组（DSS+HFD组），每组12只。采用体质量差值、疾病活动指数（DAI）和结肠组织病理学结果评估小鼠一般情况和结肠组织炎症程度，采用ELISA检测小鼠血清炎性细胞因子水平，采用实时PCR检测小鼠结肠组织中NF-κB和LC3 mRNA的表达情况。结果 DSS+HFD组体质量差值小于Control组和DSS组（均P<0.05）。DSS+HFD组DAI、结肠组织病理学评分大于Control组和DSS组（均P<0.05）。DSS+HFD组血清白细胞介素（IL）-6、肿瘤坏死因子-α （TNF-α）以及结肠组织NF-κB mRNA水平高于Control组和DSS组（均P<0.05）。DSS+HFD组结肠组织LC3 mRNA水平低于Control组和DSS组（均P<0.05）。DSS+HFD组血清IL-10水平低于Control组（P<0.05）。结论自噬在溃疡性结肠炎中起抗炎作用，高脂饮食下NF-κB抑制自噬的表达，加重结肠炎症反应。

高脂饮食下核因子κB调控自噬在小鼠溃疡性结肠炎中的作用及其机制

王钦, 刘维新, 李冬, 张慧玲, 袁琳琳, 海双双, 彭娜

中国医科大学附属第一医院消化内科, 沈阳 110001

收稿日期:2021-11-01出版日期:2022-05-30发布日期:2022-05-28
通讯作者:刘维新
作者简介:王钦(1996-),女,硕士研究生.
基金资助:辽宁省自然科学基金（20180530043）


关键词: 高脂饮食, 核因子κB, 自噬, 溃疡性结肠炎
Abstract: Objective To observe the role and underlying mechanism of nuclear factor-κB (NF-κB) in regulating autophagy in mice with dextran sulfate sodium (DSS)-induced ulcerative colitis on a high-fat diet. Methods Mice were randomly divided into normal control (Control),high-fat diet (HFD),DSS,and DSS + high-fat diet (DSS+HFD) groups (n=12 per group). The body mass difference,disease activity index (DAI),and colonic histopathological results were used to evaluate the general condition and the degree of colonic inflammation in mice. ELISA was used to detect the serum level of inflammatory factors. The expression of NF-κB and LC3 mRNA in the colon tissue was detected by real-time PCR. Results The difference in body mass was less in the DSS + HFD group than in the Control and DSS groups (all P< 0.05). The DAI and colon histopathology scores were higher in the DSS+HFD group than in the Control and DSS groups (all P< 0.05). The levels of serum interleukin (IL) -6,tumor necrosis factor-α (TNF-α),and colonic NF-κB mRNA were higher in the DSS+HFD group than in the Control and DSS groups (all P< 0.05). The expression of colonic LC3 mRNA was lower in the DSS+HFD group than in Control and DSS groups (all P< 0.05). The serum level of IL-10 was lower in DSS+HFD group than in the Control group (P< 0.05). Conclusion Autophagy plays an anti-inflammatory role in ulcerative colitis. The inhibition of autophagy by NF-κB under high-fat diet aggravates colonic inflammation.
Key words: high-fat diet, nuclear factor-κB, autophagy, ulcerative colitis
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