Lentinan extends lifespan and increases oxidative stress resistance through DAF-16 and SKN-1 pathways in Caenorhabditis elegans

Abstract

Lentinan, extracted from Lentinus edodes, exhibits bioactive properties in vitro; however, little is known about the antioxidant potential in vivo. In this study, the effects of lentinan at 0.05, 0.25 and 1.25 mg/mL on the lifespan, locomotion, reproductive capacity, and oxidative stress resistance in Caenorhabditis elegans were determined. Compared to the untreated control, lentinan at 0.05, 0.25 and 1.25 mg/mL significantly prolonged the lifespan by 17.6%, 35.3% and 25.3% (p < 0.001), respectively, and improved the brood size, locomotion and stress resistance of the nematodes. Furthermore, lentinan at 0.25 mg/mL significantly reduced accumulation of intracellular reactive oxygen species (ROS) and malondialdehyde (MDA) by 38.1% (p = 0.013) and 49.7% (p = 0.028), respectively. In addition, lentinan at all tested concentrations significantly increased the activities of superoxide dismutase (SOD) and catalase (CAT). The expression of skn-1 and daf-16 in the treatments with lentinan at 0.25 and 1.25 mg/mL was significantly (p < 0.005) up-regulated compared with the untreated control, whereas that of the daf-2 gene was significantly down-regulated. Further evidence revealed that ROS production in lentinan-treated daf-16 and skn-1 mutant strains was similar to the untreated control. Consistent with the aforementioned results, lentinan enhanced the nuclear translocation of DAF-16 and SKN-1. Our results demonstrated that lentinan could increase lifespan and protect the nematodes from oxidative stress through DAF-16 and SKN-1.