This study aimed to explore comprehensively the biological function of curcumin, and its underlying mechanism, in protecting from necrotising microscopic colitis in newborn rats. A total of 20 normal healthy rats were selected, and a necrotising enterocolitis (NEC) model was established. After hypoxia and hypothermia stimulation, these rats were treated with different doses of curcumin (control group, NEC model group, NEC+20 mg/kg curcumin and NEC+50 mg/kg curcumin). Inflammation was identified using hematoxylin and eosin staining, and inflammatory factors were detected via ELISA. The mRNA and protein levels of SIRT1, NRF2, TLR4, NLRP3 and caspase-1 were determined by quantitative RT-PCR and Western blotting, respectively. Curcumin improved the inflammatory condition of NEC and inhibited the expression of inflammatory factors in NEC newborn rat intestinal tissue. Furthermore, the SIRT1/NRF2 pathway was inhibited in the intestinal tissue of NEC newborn rats, whereas curcumin treatment induced the activation of the SIRT1/NRF2 pathway and inhibited TLR4 expression in these animals. In addition, curcumin could also inhibit the expression of inflammatory factors and alleviate the LPS/ATP-induced focal death pathway in intestinal epithelial cells through the SIRT1 pathway. Curcumin can improve necrotising microscopic colitis and cell pyroptosis by attenuating NEC-induced inhibition of SIRT1/NRF2 and inhibiting the TLR4 signalling pathway in newborn rats.

本研究旨在全面探讨姜黄素在预防新生大鼠坏死性微观结肠炎中的生物学功能及其潜在机制。共选择正常健康大鼠20只，建立坏死性小肠结肠炎（NEC）模型。缺氧低温刺激后，给予不同剂量姜黄素治疗（对照组、NEC模型组、NEC+20 mg/kg姜黄素和NEC+50 mg/kg姜黄素）。使用苏木精和伊红染色鉴定炎症，并通过ELISA检测炎症因子。分别通过定量 RT-PCR 和蛋白质印迹法测定 SIRT1、NRF2、TLR4、NLRP3 和 caspase-1 的 mRNA 和蛋白质水平。姜黄素改善NEC的炎症状态，抑制NEC新生大鼠肠道组织炎症因子的表达。此外，NEC 新生大鼠肠道组织中的 SIRT1/NRF2 通路被抑制，而姜黄素处理诱导了这些动物的 SIRT1/NRF2 通路的激活并抑制了 TLR4 的表达。此外，姜黄素还可通过SIRT1通路抑制炎症因子的表达，减轻LPS/ATP诱导的肠上皮细胞局灶性死亡通路。姜黄素可通过减弱 NEC 诱导的 SIRT1/NRF2 抑制和抑制新生大鼠 TLR4 信号通路来改善坏死性微观结肠炎和细胞焦亡。而姜黄素治疗会诱导 SIRT1/NRF2 通路的激活并抑制这些动物的 TLR4 表达。此外，姜黄素还可通过SIRT1通路抑制炎症因子的表达，减轻LPS/ATP诱导的肠上皮细胞局灶性死亡通路。姜黄素可通过减弱 NEC 诱导的 SIRT1/NRF2 抑制和抑制新生大鼠 TLR4 信号通路来改善坏死性微观结肠炎和细胞焦亡。而姜黄素治疗会诱导 SIRT1/NRF2 通路的激活并抑制这些动物的 TLR4 表达。此外，姜黄素还可通过SIRT1通路抑制炎症因子的表达，减轻LPS/ATP诱导的肠上皮细胞局灶性死亡通路。姜黄素可通过减弱 NEC 诱导的 SIRT1/NRF2 抑制和抑制新生大鼠 TLR4 信号通路来改善坏死性微观结肠炎和细胞焦亡。