Forsythia suspensa extract attenuates lipopolysaccharide‐induced inflammatory liver injury in rats via promoting antioxidant defense mechanisms. (17th October 2016)

• Record Type: Journal Article
• Authors: Zhao, Panfeng; Piao, Xiangshu; Pan, Long; Zeng, Zhikai; Li, Qingyun; Xu, Xiao; Wang, Hongliang
• Is Part Of: Animal science journal. Volume 88:Number 6(2017:Jun.)
• Page Start: 873
• Page End: 881
• Publication Date: 2016-10-17
• Subjects: Forsythia suspensaextract -- inflammatory liver injury -- inflammatory response -- lipopolysaccharide -- oxidative stress; Animal culture -- Periodicals; Livestock -- Periodicals; 636
• DOI: 10.1111/asj.12717
• Languages: English
• ISSNs: 1344-3941

Abstract

Abstract: Reactive oxygen species (ROS) have been shown to have a role in inflammation. We investigated whether Forsythia suspensa extract (FSE) could exert its antioxidant potential against lipopolysaccharide (LPS)‐induced inflammatory liver injury in rats. Rats were orally fed FSE once daily for 7 consecutive days prior to LPS ( Escherichia coli, serotype O55:B5) injection. LPS treatment caused liver dysfunction as evidenced by massive histopathological changes and increased serum alanine aminotransferase and aspartate aminotransferase activities which were ameliorated by FSE pretreatment. FSE attenuated LPS‐induced depletion of cytosolic nuclear factor‐erythroid 2‐related factor 2 (Nrf2) and suppression of Nrf2 nuclear translocation in liver, and the generation of ROS and malondialdehyde in serum and liver. FSE increased the Nrf2‐mediated induction of heme oxygenase‐1 in liver, as well as superoxide dismutase and glutathione peroxidase activities in serum and liver. Importantly, FSE attenuated LPS‐induced nuclear factor‐кB (NF‐кB) nuclear translocation in liver, and subsequently decreased tumor necrosis factor‐α, interleukin (IL)‐1β and IL‐6 levels in serum and liver, which were associated with FSE‐induced activation of Nrf2 in liver. These results indicate that the protective mechanisms of FSE may be involved in the attenuation of oxidative stress and the inhibition of the NF‐кB‐mediated inflammatory response by modulating the Nrf2‐mediated antioxidant response against LPS‐induced inflammatory liver injury.