Surgery for colorectal cancer (CRC) can cause damage to the intestinal mucosal barrier and lead to bacterial invasion. This study mainly analyzed whether propofol (PPF) could protect the intestinal mucosal barrier damage caused by CRC surgery, and explored its molecular mechanism. A mouse CRC model was constructed using azomethane and dextran sulfate sodium. During anesthesia, continuous intravenous injection of PPF was used for intervention. The influences of PPF on intestinal mucosal permeability and bacterial invasion were detected. The levels of microRNA (miR)-155, Toll-like receptor 4 (TLR4)/NF-κB in the intestinal mucosa, and the location of miR-155 were detected by fluorescence in situ hybridization (FISH). Mouse macrophages were used to analyze the regulation of miR-155 on the secretion of inflammatory cytokines through the TLR4/NF-κB pathway. PPF treatment promoted the expression of tight junction protein in the intestinal mucosa, protected the intestinal barrier, inhibited the translocation of intestinal bacteria, and increased the level of the beneficial bacterium Lactobacillus on the mucosal surface. In addition, PPF treatment could inhibit the expression of miR-155, TLR4/NF-KB, and reverse inflammatory response. miR-155 was expressed in macrophages of intestinal mucosa tissue. Overexpression of miR-155 promoted the nuclear translocation of NF-κB and the expression of inflammatory cytokines in macrophages. The use of VIPER to inhibit TLR4 reversed the pro-inflammatory effects of miR-155. PPF might inhibit the activation of the NF-κB pathway by downregulating miR-155 expression, thereby reducing the secretion of inflammatory cytokines. This might be the mechanism by which PPF protected the intestinal barrier of CRC surgical model mice.

结直肠癌 (CRC) 手术可导致肠黏膜屏障受损并导致细菌入侵。本研究主要分析丙泊酚（PPF）是否能够保护结直肠癌手术引起的肠黏膜屏障损伤，并探讨其分子机制。使用偶氮甲烷和葡聚糖硫酸钠构建小鼠CRC模型。麻醉期间采用持续静脉注射PPF进行干预。检测了PPF对肠黏膜通透性和细菌侵袭的影响。荧光原位检测肠黏膜中microRNA（miR）-155、Toll样受体4（TLR4）/NF-κB的水平及miR-155的定位杂交（FISH）。小鼠巨噬细胞用于分析 miR-155 通过 TLR4/NF-κB 通路对炎性细胞因子分泌的调节作用。PPF处理促进了肠黏膜紧密连接蛋白的表达，保护了肠道屏障，抑制了肠道细菌的易位，提高了有益菌乳酸杆菌的水平在黏膜表面。此外，PPF 治疗可以抑制 miR-155、TLR4/NF-KB 的表达，并逆转炎症反应。miR-155 在肠黏膜组织的巨噬细胞中表达。miR-155的过表达促进了NF-κB的核转位和巨噬细胞中炎性细胞因子的表达。使用 VIPER 抑制 TLR4 可逆转 miR-155 的促炎作用。PPF 可能通过下调 miR-155 的表达来抑制 NF-κB 通路的激活，从而减少炎性细胞因子的分泌。这可能是PPF保护CRC手术模型小鼠肠道屏障的机制。