title: Sargassum fusiforme polysaccharides activate antioxidant defense by promoting Nrf2-dependent cytoprotection and ameliorate stress insult during aging.
abstract: Aging is a complex issue, which results in a progressive decline process in cellular protection and physiological functions. Illustrating the causes of aging and pharmaceutical interference with the aging process has been a pivotal issue for thousands of years. Sargassum fusiforme (S. fusiforme), a kind of brown alga, is also named the "longevity vegetable" as it is not only a kind of food, but also used as an herb in traditional Chinese Medicine for maintaining health and treatment of thyroid disease, cardiovascular disease and so on. But how S. fusiforme promotes longevity is vastly equivocal. We got clues from S. fusiforme polysaccharides, which exhibited antioxidant activity, but the underlying mechanisms remained unclear. In this study, we evaluated the antioxidant effect and the possible mechanisms that S. fusiforme polysaccharides have against d-galactose-induced aging and chronic aging. We selected the SFPS as the candidate for antioxidant defense evaluation, which is a type of S. fusiforme polysaccharide with strong free radical scavenging activity and non-toxicity. It revealed that the antioxidant defense of the d-galactose-induced mice was markedly recovered when they were intragastrically administrated with the SFPS. However, oxidative damage may not be the only cause of aging. We further evaluated the function of the SFPS in the chronic aging mice. Intriguingly, we even found an obvious aging phenotype in the middle aged male ICR mice, which showed a significant decline in Nrf2-dependent cytoprotection. When 9-month old male ICR mice were treated with the SFPS for 2 months or even 11 months to their mean survival age, experimental measurements showed that the SFPS significantly promoted the antioxidant defense and mitochondrial integrity during aging. Furthermore, we suggest that the SFPS promotes Nrf2-dependent cytoprotection by upregulating the nuclear Nrf2 translocation, which may be mediated by p21 and JNK dependent pathways. These results suggest that the SFPS may decelerate the aging process by enhancing Nrf2-dependent cytoprotection, especially antioxidant defense.
authors.affiliation: College of Life and Environmental Science, Wenzhou University, Wenzhou 325035, P.R. China and WZU&WMU Collaborative Innovation Center of Biomedicine, Wenzhou 325035, P.R. China. wumingjiangwz@163.com zhangxu419@126.com.
authors.forename: Peichao
authors.initials: P
authors.lastname: Chen
authors.affiliation: College of Life and Environmental Science, Wenzhou University, Wenzhou 325035, P.R. China.
authors.forename: Dan
authors.initials: D
authors.lastname: He
authors.affiliation: College of Life and Environmental Science, Wenzhou University, Wenzhou 325035, P.R. China.
authors.forename: Ya
authors.initials: Y
authors.lastname: Zhang
authors.affiliation: College of Life and Environmental Science, Wenzhou University, Wenzhou 325035, P.R. China.
authors.forename: Shanshan
authors.initials: S
authors.lastname: Yang
authors.affiliation: College of Life and Environmental Science, Wenzhou University, Wenzhou 325035, P.R. China.
authors.forename: Liujun
authors.initials: L
authors.lastname: Chen
authors.affiliation: College of Life and Environmental Science, Wenzhou University, Wenzhou 325035, P.R. China and WZU&WMU Collaborative Innovation Center of Biomedicine, Wenzhou 325035, P.R. China. wumingjiangwz@163.com zhangxu419@126.com.
authors.forename: Shengqin
authors.initials: S
authors.lastname: Wang
authors.affiliation: College of Life and Environmental Science, Wenzhou University, Wenzhou 325035, P.R. China and WZU&WMU Collaborative Innovation Center of Biomedicine, Wenzhou 325035, P.R. China. wumingjiangwz@163.com zhangxu419@126.com.
authors.forename: Huixi
authors.initials: H
authors.lastname: Zou
authors.affiliation: College of Life and Environmental Science, Wenzhou University, Wenzhou 325035, P.R. China and WZU&WMU Collaborative Innovation Center of Biomedicine, Wenzhou 325035, P.R. China. wumingjiangwz@163.com zhangxu419@126.com.
authors.forename: Zhiyong
authors.initials: Z
authors.lastname: Liao
authors.affiliation: College of Life and Environmental Science, Wenzhou University, Wenzhou 325035, P.R. China and WZU&WMU Collaborative Innovation Center of Biomedicine, Wenzhou 325035, P.R. China. wumingjiangwz@163.com zhangxu419@126.com.
authors.forename: Xu
authors.initials: X
authors.lastname: Zhang
authors.affiliation: College of Life and Environmental Science, Wenzhou University, Wenzhou 325035, P.R. China and WZU&WMU Collaborative Innovation Center of Biomedicine, Wenzhou 325035, P.R. China. wumingjiangwz@163.com zhangxu419@126.com.
authors.forename: Mingjiang
authors.initials: M
authors.lastname: Wu
mesh_terms: D000375:Aging / Q000187:drug effects*; D000818:Animals; D002460:Cell Line; D019610:Cytoprotection / Q000187:drug effects; D005260:Female; D005786:Gene Expression Regulation / Q000187:drug effects*; D022781:Hepatocytes / Q000187:drug effects; D006801:Humans; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D051267:NF-E2-Related Factor 2 / Q000378:metabolism*; D011134:Polysaccharides / Q000737:chemistry* / Q000494:pharmacology*; D011897:Random Allocation; D044647:Sargassum / Q000737:chemistry*; D013312:Stress, Physiological; D015854:Up-Regulation
chemical_list: D051267:NF-E2-Related Factor 2; C495635:NFE2L2 protein, human; D011134:Polysaccharides