Ameliorative effect of ampelopsin on LPS-induced acute phase response in piglets. (August 2017)

• Record Type: Journal Article
• Authors: Hou, Xiang; Wang, Tian; Ahmad, Hussain; Xu, Ziwei
• Is Part Of: Journal of functional foods. Volume 35(2017)
• Page Start: 489
• Page End: 498
• Publication Date: 2017-08
• Subjects: APR acute phase response -- APS Ampelopsin -- NF-κB nuclear factor kappa B -- Nrf2 NF-E2-related nuclear factor 2 -- ROS reactive oxygen species -- Ref-1 Redox factor-1 -- STAT3 signal transduction and transcription 3; Acute phase response -- Ampelopsin -- Inflammation -- Cellular redox state -- Mitochondrial dysfunction; Functional foods -- Analysis -- Periodicals; Food -- Biotechnology -- Periodicals; Nutrition -- Periodicals; 613.2
• DOI: 10.1016/j.jff.2017.05.044
• Languages: English
• ISSNs: 1756-4646

Abstract

Graphical abstract: Highlights: Ampelopsin supplementation modulates whole-body energy metabolic and physical conditions in APR. Ampelopsin supplementation suppresses inflammatory mediators in APR. Ampelopsin supplementation ameliorates liver mitochondrial dysfunction in APR. Ampelopsin supplementation restores altered liver redox state in APR. Abstract: Ampelopsin (APS) is the main bioactive component from Ampelopsis grossedentata and has anti-inflammatory properties. We hypothesize that it could reduce the acute phase response (APR) and help to maintain balance between inflammation-mediated oxidative damage and APS-induced protective mechanisms in liver. In the present study, APS possessed strong DPPH, ABTS, H2 O2 and O 2 radical scavenging activities in different in vitro antioxidant assays. Further study demonstrated that APS alleviated APR as reflected in the changes in the whole body metabolic rate, physical conditions, and production of cytokines in LPS-treated piglets. Moreover, APS has the potential to prevent Akt-mediated activation of NF-κB and decreased the levels of STAT3 in inflammation. The administration of APS ameliorated mitochondrial dysfunction and moderated the involvement of Ref-1 and Nrf2 in the attenuation in LPS-induced APR. The present results suggest that the APS attenuate LPS induced inflammation and oxidative stress in liver of piglets.