Long-term schisandrin B treatment mitigates age-related impairments in mitochondrial antioxidant status and functional ability in various tissues, and improves the survival of aging C57BL/6J mice

• Published in: BioFactors (Oxford) Vol. 34; no. 4; pp. 331 - 342
• Main Authors: Ko, Kam Ming, Chen, Na, Leung, Hoi Yan, Leong, Eriol P. K., Poon, Michel K. T., Chiu, Po Yee
• Format: Journal Article
• Language: English
• Published: Amsterdam IOS Press 2008
• Subjects: aging; Aging - drug effects; Aging - metabolism; Animals; Antioxidants - metabolism; ATP generation; brain; Brain - drug effects; Brain - metabolism; Cyclooctanes - administration & dosage; Cyclooctanes - pharmacology; Dietary Supplements; Female; Glutathione; heart; Heart - drug effects; kidney; Kidney - drug effects; Kidney - metabolism; Lignans - administration & dosage; Lignans - pharmacology; liver; Liver - drug effects; Liver - metabolism; Male; Mice; Mice, Inbred C57BL; mitochondria; Mitochondria - drug effects; Mitochondria - metabolism; Mn-superoxide dismutase; Oxidative Stress - drug effects; Polycyclic Compounds - administration & dosage; Polycyclic Compounds - pharmacology; reactive oxygen species; Schisandra; Schisandrin B; Superoxide Dismutase - metabolism; α-tocopherol
• ISSN: 0951-6433; 1872-8081
• DOI: 10.1002/biof.5520340408

Mitochondrial decay is a major cause of aging, leading to the subsequent death of aerobic organisms including humans. In the present study, we examined the effects of supplementation with schisandrin B (Sch B, a dibenzocyclooctadiene derivative isolated from the fruit of Schisandra chinensis), administered at 0.012% (w/w) of diet, starting from the age of 36 weeks, on age‐dependent changes in mouse mitochondrial antioxidant status and functional ability in various tissues (brain, heart, liver, and kidney) up to the age of 120 weeks. We also monitored survival of male and female C57BL/6J mice. Aging caused progressive impairment in mitochondrial antioxidant status in various tissues, as evidenced by decreases in reduced glutathione and α‐tocopherol levels, and Mn‐superoxide dismutase activity. Impairments in mitochondrial antioxidant status were invariably associated with increases in mitochondria‐driven reactive oxygen species (ROS) production in tissue homogenates, as well as decreased mitochondrial ATP‐generation capacities (ATP‐GCs), in all tested tissues. Diet supplementation with Sch B ameliorated impairment in mitochondrial antioxidant status during aging. The effects were more pronounced in younger than in older mice, when compared to age‐matched non‐supplemented controls. Sch B supplementation also suppressed mitochondria‐driven ROS production and enhanced mitochondrial ATP‐GC in various tissues during aging. The beneficial effects of Sch B supplementation on mitochondrial antioxidant status and functional ability were paralleled by survival improvement in aging male mice, when compared with controls. Sch B supplementation also improved the survival in female mice. In conclusion, long‐term Sch B supplementation mitigated age‐dependent impairments in mitochondrial antioxidant capacity and functional ability, thereby retarding the aging process in mice, particularly during early aging.