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