Sulforaphane ameliorates cadmium induced hepatotoxicity through the up-regulation of /Nrf2/ARE pathway and the inactivation of NF-κB. (February 2021)

• Record Type: Journal Article
• Authors: He, Qingfeng; Luo, Yunjing; Xie, Ziqi
• Is Part Of: Journal of functional foods. Volume 77(2021)
• Publication Date: 2021-02
• Subjects: Cadmium -- Sulforaphen -- Hepatotoxicity -- Oxidative stress -- Inflammation; ABTS 2, 2-Azinobis-(3-ethylbenzthiazoline-6-sulphonate) -- ARE antioxidant response element -- CAT catalase -- Cd cadmium -- GSH reduced glutathione -- HO-1 hemeoxygenase-1 -- IL-1β interleukin 1β -- MDA malondialdehyde -- NF-κB nuclear factor-kappa B -- ONOO− peroxynitrite -- SFN sulforaphane -- TAC total antioxidant capacity -- TNF-α tumor necrosis factor-α -- ALT alanine aminotransferase -- AST aspartate aminotransferase -- CdCl2 cadmium chloride -- DPPH 1, 1-diphenyl-2-picrylhydrazyl -- GST glutathione S-transferase -- IL-6 interleukin 6 -- Keap-1 kelch-like-ECH-associated protein-1 -- MTT 3-(4, 5-Dimethylthiazol-2-yl)-2, 5, diphenyl-tetrazolium bromide -- Nrf2 nuclear factor-E2-related factor 2 -- ROS reactive oxygen species -- SOD superoxide dismutase -- TBil total bilirubin; Functional foods -- Analysis -- Periodicals; Food -- Biotechnology -- Periodicals; Nutrition -- Periodicals; 613.2
• DOI: 10.1016/j.jff.2020.104297
• Languages: English
• ISSNs: 1756-4646

Abstract

Graphical abstract: Highlights: SFN effectivelly scavenges free radicals and ROS induced by cadmium. Antioxidation and anti-inflammation contribute to the hepatoprotection of SFN. SFN ameliorates Cd induced antioxidative stress by regulation of Nrf2/ARE pathway. NF-κB inactivion by SFN mostly facilitates the up-regulation of Nrf2 signal. Abstract: This study aimed to assess the ameliorative effect and mechanisms of sulforaphane (SFN) on cadmium (Cd)-induced hepatotoxicity. Four in vitro free radical scavenging tests, HepG2 cell viability analysis, and cadmium chloride (CdCl2 ) indeced liver injured mice mode were employed. SFN scavenged the free radicals in vitro, and mitigated the oxidative damages in HepG2 cells incubated with SFN + CdCl2 . In mice models, SFN pretreatment dose-dependently remarkably improved redox homeostasis, and attenuated the expressions of the key liver inflammatory factors (TNF-α, IL-6, IL-1β) by CdCl2 . The pathological examinations were consistent with the above results. Moreover, both mRNA and protein expression of hepatic nuclear factor-erythroid 2-related factor 2 and hemeoxygenase-1 increased, while nuclear factor-kappa B reduced in Cd + SFN co-treated groups. Taken together, this study firstly demonstrated the anti-oxidant and anti-inflammatory effects of SFN against Cd induced liver damages, which associated with the modulation of intrinsic Nrf2/ARE and NF-κB pathway.