Zhu Chenghui, Zhang Shuimei, Song Chengwei, Zhang Yibo, Ling Qinjie, Hoffmann Peter R, Li Jun, Chen Tianfeng, Zheng Wenjie, Huang Zhi
School of Life Science and Technology, Jinan University, Guangzhou, 510632, Guangdong Province, China.
College of Pharmacy, Jinan University, Guangzhou, 510632, Guangdong Province, China.
J Nanobiotechnology. 2017 Mar 7;15(1):20. doi: 10.1186/s12951-017-0252-y.
Selenium (Se) is an essential micronutrient trace element and an established nutritional antioxidant. Low Se status exacerbates inflammatory bowel diseases progression, which involves hyper inflammation in the digestive tract. Se nanoparticles (SeNPs) exhibit anti-inflammatory activity accompanied by low toxicity, especially when decorated with natural biological compounds. Herein, we explored the beneficial effects of SeNPs decorated with Ulva lactuca polysaccharide (ULP) in mice subjected to the acute colitis model.
We constructed SeNPs coated with ULP (ULP-SeNPs) in average diameter ~130 nm and demonstrated their stability and homogeneity. Supplementation with ULP-SeNPs (0.8 ppm Se) resulted in a significant protective effect on DSS-induced acute colitis in mice including mitigation of body weight loss, and colonic inflammatory damage. ULP-SeNPs ameliorated macrophage infiltration as evidenced by decreased CD68 levels in colon tissue sections. The anti-inflammatory effects of ULP-SeNPs were found to involve modulation of cytokines including IL-6 and TNF-α. Mechanistically, ULP-SeNPs inhibited the activation of macrophages by suppressing the nuclear translocation of NF-κB, which drives the transcription of these pro-inflammatory cytokines.
ULP-SeNPs supplementation may offer therapeutic potential for reducing the symptoms of acute colitis through its anti-inflammatory actions.
硒(Se)是一种必需的微量营养元素,也是一种公认的营养抗氧化剂。低硒状态会加剧炎症性肠病的进展,这涉及消化道的过度炎症。硒纳米颗粒(SeNPs)具有抗炎活性且毒性较低,尤其是当用天然生物化合物修饰时。在此,我们探讨了用石莼多糖(ULP)修饰的SeNPs对急性结肠炎模型小鼠的有益作用。
我们构建了平均直径约130nm的ULP包被的SeNPs(ULP-SeNPs),并证明了它们的稳定性和均匀性。补充ULP-SeNPs(0.8ppm硒)对右旋糖酐硫酸钠(DSS)诱导的小鼠急性结肠炎具有显著的保护作用,包括减轻体重减轻和结肠炎症损伤。结肠组织切片中CD68水平降低证明ULP-SeNPs改善了巨噬细胞浸润。发现ULP-SeNPs的抗炎作用涉及对包括白细胞介素-6(IL-6)和肿瘤坏死因子-α(TNF-α)在内的细胞因子的调节。从机制上讲,ULP-SeNPs通过抑制驱动这些促炎细胞因子转录的核因子-κB(NF-κB)的核转位来抑制巨噬细胞的激活。
补充ULP-SeNPs可能通过其抗炎作用为减轻急性结肠炎症状提供治疗潜力。