Issue 14, 2022

Lycopene attenuates d-galactose-induced insulin signaling impairment by enhancing mitochondrial function and suppressing the oxidative stress/inflammatory response in mouse kidneys and livers

Abstract

Lycopene (LYC) possesses bioactivity to improve the pathogenesis of several chronic diseases via antioxidant-associated mechanisms. The purpose of this study was to investigate whether LYC could attenuate D-galactose (D-gal)-induced mitochondrial dysfunction and insulin signaling impairment in mouse kidneys and livers. Two-month-old CD-1 mice were treated by intraperitoneal injection of 150 mg kg−1 day−1D-gal for 8 weeks and received 0.03% LYC (w/w, mixed into diet). The results showed that LYC ameliorated oxidative stress triggered by D-gal by enhancing the Nrf2 antioxidant defense pathway and increasing the expression of the antioxidant response genes HO-1 and NQO1 in mouse kidneys and livers. LYC inhibited the MAPK and NFκB pathways and attenuated renal and hepatic inflammatory responses. Moreover, LYC upregulated the expression of genes related to mitochondrial biosynthesis and oxidative phosphorylation and improved insulin signal transduction through the IRS-1/AKT/GSK3β pathway in mouse kidneys and livers.

Graphical abstract: Lycopene attenuates d-galactose-induced insulin signaling impairment by enhancing mitochondrial function and suppressing the oxidative stress/inflammatory response in mouse kidneys and livers

Article information

Article type
Paper
Submitted
12 Mar 2022
Accepted
30 May 2022
First published
02 Jun 2022

Food Funct., 2022,13, 7720-7729

Lycopene attenuates D-galactose-induced insulin signaling impairment by enhancing mitochondrial function and suppressing the oxidative stress/inflammatory response in mouse kidneys and livers

J. Wang, T. Li, M. Li, D. Shi, X. Tan and F. Qiu, Food Funct., 2022, 13, 7720 DOI: 10.1039/D2FO00706A

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