Key Laboratory for Animal Disease-Resistance Nutrition of China Ministry of Education, Institute of Animal Nutrition, Sichuan Agricultural University, Chengdu, Sichuan 611130, P. R. China.
Food Funct. 2023 Feb 6;14(3):1617-1626. doi: 10.1039/d2fo03586c.
The aim of this study was to investigate the effect of naringin on lipopolysaccharide (LPS)-induced jejunal barrier function in mice. Forty-five 3-week-old healthy male Balb/c mice with similar body weights were randomly divided into control group, LPS group, LPS + naringin group, with 15 mice in each treatment group. The mice were intraperitoneally injected with the same dose of saline or LPS (10 mg per kg BW) at 43 d. The blood samples, liver and jejunal tissues were collected after 3 h of injection. The results showed that LPS significantly increased the serum diamine oxidase (DAO) activity, D-lactate (D-LA) concentration, and malondialdehyde (MDA) content in liver and jejunum, while decreased the activities of superoxide dismutase (SOD), glutathione peroxidase (Gpx) and catalase (CAT) in liver and jejunum. The LPS treatment caused an increase in the crypt depth and a decrease in the villus height and the ratio of villus height to crypt depth (V/C) of the jejunum. In addition, the LPS treatment significantly increased the mRNA expressions of tumor necrosis factor-α (), interleukin-1β (), , toll-like receptor 4 (), p38-mitogen-activated protein kinase (), nuclear factor-κB () and kelch-like ECH-associated protein 1 (), while decreased mRNA expressions of zonula occludens 1 (), , , mucin 2 () and junctional adhesion molecule 2 (), , , , and nuclear factor-erythroid 2-related factor 2 (). However, the naringin treatment mitigated these effects induced by LPS. Taken together, our findings suggested that naringin attenuates LPS-induced intestinal barrier damage by inhibiting inflammatory factors and improving antioxidant function and intestinal tight junction, which might be mediated by activating the Nrf2 signaling and suppressing the TLR4/p38 MAPK/NF-κB signaling.
本研究旨在探讨柚皮苷对脂多糖（LPS）诱导的小鼠空肠屏障功能的影响。将 45 只 3 周龄、体重相近的健康雄性 Balb/c 小鼠随机分为对照组、LPS 组、LPS+柚皮苷组，每组 15 只。第 43 天，各组小鼠均经腹腔注射等剂量生理盐水或 LPS（10mg/kg BW）。注射后 3h 采集血样、肝脏和空肠组织。结果显示，LPS 显著增加了肝脏和空肠组织中二胺氧化酶（DAO）活性、D-乳酸（D-LA）浓度和丙二醛（MDA）含量，同时降低了肝脏和空肠组织中超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（Gpx）和过氧化氢酶（CAT）活性。LPS 处理增加了空肠隐窝深度，降低了绒毛高度和绒毛高度与隐窝深度的比值（V/C）。此外，LPS 处理显著增加了肿瘤坏死因子-α（）、白细胞介素-1β（）、白细胞介素-6（）、Toll 样受体 4（）、p38-丝裂原活化蛋白激酶（p38-MAPK）、核因子-κB（）和Kelch 样 ECH 相关蛋白 1（Keap1）mRNA 的表达，同时降低了紧密连接蛋白 1（）、闭锁小带蛋白 1（）、Occludin 蛋白 1（）、黏蛋白 2（）、JAM2 蛋白 1（）和核因子-红细胞 2 相关因子 2（Nrf2）mRNA 的表达。然而，柚皮苷处理减轻了 LPS 诱导的这些作用。综上所述，本研究结果表明，柚皮苷通过抑制炎症因子、改善抗氧化功能和肠道紧密连接来减轻 LPS 诱导的肠道屏障损伤，其机制可能与激活 Nrf2 信号通路和抑制 TLR4/p38 MAPK/NF-κB 信号通路有关。
