Department of Neonatology, Children's Hospital of Chongqing Medical University, Chongqing, China.
National Clinical Research Center for Child Health and Disorders, Chongqing, China.
Mediators Inflamm. 2021 Oct 12;2021:6259381. doi: 10.1155/2021/6259381. eCollection 2021.
To determine the role of sodium butyrate in intestinal inflammation via regulation of high-mobility group box-1 (HMGB1), we analyzed the potential mechanism in necrotizing enterocolitis (NEC) in a neonatal mouse model.
A NEC model was created with hypoxia and cold exposure and artificial overfeeding. C57BL/6 neonatal mice were randomized into three groups: the control, untreated NEC, and sodium butyrate (150 mM)-pretreated NEC groups. Pathological variations in ileocecal intestinal tissue were observed by HE staining and scored in a double-blind manner. The mRNA expression levels of HMGB1, Toll-like receptor 4 (TLR4), nuclear factor-B (NF-B), and inflammatory cytokines in intestinal tissues were determined by quantitative real-time PCR. The protein levels of HMGB1 and associated cytokines in intestinal tissues were evaluated using ELISA. The relative protein expression levels of TLR4 and NF-B in intestinal tissues were quantified by western blot.
Sodium butyrate administration improved the body weight and survival rate of NEC mice; relieved intestinal pathological injury; reduced the intestinal expression of HMGB1, TLR4, NF-B, interleukin- (IL-) 1, IL-6, IL-8, and TNF-; and increased the intestinal expression of IL-10 ( < 0.05). Treatment with butyrate decreased the proportion of opportunistic and and increased the proportion of beneficial and in the NEC model.
Sodium butyrate intervention relieves intestinal inflammation and partially corrects the disrupted intestinal flora in mice with NEC.
通过调控高迁移率族蛋白 B1（HMGB1），确定丁酸钠在肠道炎症中的作用，我们分析了新生鼠坏死性小肠结肠炎（NEC）模型中的潜在机制。
采用低氧冷暴露和人工过度喂养建立 NEC 模型。将 C57BL/6 新生小鼠随机分为三组：对照组、未治疗 NEC 组和丁酸钠（150 mM）预处理 NEC 组。通过 HE 染色和双盲评分观察回盲肠肠组织的病理变化。采用实时定量 PCR 测定肠组织中 HMGB1、Toll 样受体 4（TLR4）、核因子-B（NF-B）和炎症细胞因子的 mRNA 表达水平。采用 ELISA 测定肠组织中 HMGB1 和相关细胞因子的蛋白水平。采用 Western blot 定量肠组织中 TLR4 和 NF-B 的相对蛋白表达水平。
丁酸钠给药改善了 NEC 小鼠的体重和存活率；缓解了肠道病理损伤；降低了肠道中 HMGB1、TLR4、NF-B、白细胞介素-（IL-）1、IL-6、IL-8 和肿瘤坏死因子-（TNF-）的表达；并增加了肠道中 IL-10 的表达（<0.05）。丁酸钠治疗降低了 NEC 模型中机会性 和 的比例，增加了有益的 和 的比例。
丁酸钠干预可缓解肠道炎症，并部分纠正 NEC 模型中肠道菌群的失调。
