Peng Yanqi, Zhu Jiayi, Li Yingshuo, Yue Xiqing, Peng Yanyu
Department of Food Science, College of Public Health, Shenyang Medical College, Shenyang 110034, China; College of Food Science, Shenyang Agricultural University, Shenyang 110866, China.
College of Public Health, Shenyang Medical College, Shenyang 110034, China.
Int J Biol Macromol. 2024 Nov;281(Pt 1):136206. doi: 10.1016/j.ijbiomac.2024.136206. Epub 2024 Oct 1.
Ulcerative colitis (UC), a type of inflammatory bowel disease (IBD), is a chronic recurrent inflammatory disease of the colon. Our previous findings demonstrated that almond polysaccharide (AP-1) exhibits significant anti-inflammatory activity in vitro. Therefore, this study aimed to explore the ameliorative effect of AP-1 on dextrose sodium sulfate (DSS)-induced UC mice and to elucidate its possible mechanism of action. By observing changes in body weight, fecal viscosity, stool blood, disease activity index, and colon length, we found that AP-1 attenuated inflammation. It inhibited TNF-α, IL-1β, and IL-6 while boosting anti-inflammatory IL-10 levels. Histomorphologically, AP-1 protected against DSS-induced colonic tissue damage by reducing inflammatory cell infiltration and mucosal injury. It also lowered myeloperoxidase (MPO) and NO while increasing total superoxide dismutase (T-SOD) and glutathione peroxidase (GSH-Px) in colonic tissues. Moreover, using the Western blot technique, AP-1 was shown to inhibit the phosphorylation of p65 and IκB-α proteins in the NF-κB/iNOS/COX2 signaling pathway and down-regulate the expression of inflammation-associated proteins COX2 and iNOS, thus slowing down and ameliorating inflammatory processes. Therefore, the safe and effective beneficial effects of AP-1 make it a promising therapeutic strategy for relieving IBD, especially UC.
溃疡性结肠炎(UC)是炎症性肠病(IBD)的一种,是结肠的慢性复发性炎症性疾病。我们之前的研究结果表明,杏仁多糖(AP-1)在体外具有显著的抗炎活性。因此,本研究旨在探讨AP-1对葡聚糖硫酸钠(DSS)诱导的UC小鼠的改善作用,并阐明其可能的作用机制。通过观察体重、粪便粘度、便血、疾病活动指数和结肠长度的变化,我们发现AP-1减轻了炎症。它抑制了肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)和白细胞介素-6(IL-6),同时提高了抗炎性白细胞介素-10(IL-10)的水平。从组织形态学上看,AP-1通过减少炎症细胞浸润和黏膜损伤,保护结肠组织免受DSS诱导的损伤。它还降低了结肠组织中的髓过氧化物酶(MPO)和一氧化氮(NO)水平,同时提高了总超氧化物歧化酶(T-SOD)和谷胱甘肽过氧化物酶(GSH-Px)的水平。此外,使用蛋白质印迹技术,AP-1被证明可以抑制NF-κB/iNOS/COX2信号通路中p65和IκB-α蛋白的磷酸化,并下调炎症相关蛋白COX2和iNOS的表达,从而减缓并改善炎症过程。因此,AP-1的安全有效有益作用使其成为缓解IBD,尤其是UC的一种有前景的治疗策略。