Quercetin and lycopene co-administration prevents oxidative damage induced by d-galactose in mice

Quercetin and lycopene are strong dietary antioxidants that often co-exist in foods. Here, the cardiac and neuroprotective effects of quercetin and lycopene combination were analyzed in d-galactose-induced oxidative stress in mice. ICR mice were divided into control group, d-galactose group (D-GAL), quercetin treatment (Q45: 45 mg kg−1 d−1quercetin, Q60: 60 mg kg−1 d−1 quercetin), lycopene treatment (15 mg kg−1 d−1 lycopene), and M groups (45 mg kg−1 d−1quercetin+15 mg kg−1 d−1 lycopene). Mice were given quercetin, lycopene, and their combination through oral gavage for 6 weeks. They were injected with d-galactose (150 mg kg−1 d−1) simultaneously except for the control group. Results showed that the quercetin-lycopene combination could ameliorate histopathological injuries in the heart and hippocampus. They significantly decreased the serum and heart malonaldehyde (MDA) levels, heart 4-Hydroxynonenal (4-HNE) levels, and increased the activity of serum and heart superoxide dismutase (SOD), catalase (CAT), and the hippocampal SOD and CAT mRNA level. Quercetin-lycopene combination exhibited anti-inflammation effects by reducing inflammatory genes such as cyclooxygenase-2 (COX-2) and interleukin-1β (IL-1β). The heart and hippocampal mRNA level of nuclear factor erythroid 2-related factor 2 (Nrf2) expression was up-regulated, and the antioxidant genes related to Nrf2 including heme oxygenase-1 (HO-1), NAD(P)H Quinone Dehydrogenase 1 (NQO1) were elevated. Quercetin-lycopene combination significantly promoted the mRNA level of deacetylase sirtuin-1 (SIRT1), increased 3.3-fold and 3-fold SIRT1 expression in the heart and hippocampus, respectively. They could bind SIRT1 at the active site predicted by molecular docking. These results suggested that they may interact with SIRT1 to activate Nrf2, inhibit pro-inflammatory factors, and prevent oxidative stress in D-GAL-induced mice.