Naringin mitigates LPS-induced intestinal barrier injury in mice.

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 ( TNF-α ), interleukin-1β ( IL-1β ), IL-6 , toll-like receptor 4 ( TLR4 ), p38-mitogen-activated protein kinase ( p38 MAPK ), nuclear factor-κB ( NF-κB ) and kelch-like ECH-associated protein 1 ( Keap1 ), while decreased mRNA expressions of zonula occludens 1 ( ZO-1 ), occludin , claudin , mucin 2 ( MUC2 ) and junctional adhesion molecule 2 ( JAM2 ), Gpx , SOD1 , GST , CAT and nuclear factor-erythroid 2-related factor 2 ( Nrf2 ). 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.