Chronic schisandrin B treatment improves mitochondrial antioxidant status and tissue heat shock protein production in various tissues of young adult and middle-aged rats.

The effects of chronic schisandrin B (Sch B) treatment (10 mg/kg/dayx15) on mitochondrial antioxidant status and sensitivity to Ca2+-induced permeability transition, as well as tissue heat shock protein (Hsp)25/70 production were examined in various tissues (brain, heart, liver, skeletal muscle) of young adult and middle-aged female rats. Age-dependent impairment in mitochondrial antioxidant status, as assessed by levels/activities of antioxidant components (reduced glutathione, alpha-tocopherol, Se-glutathione peroxidase and Mn-superoxide dismutase) and the extent of reactive oxygen species generation in vitro, was observed in brain, heart, liver and skeletal muscle tissues. While tissue Hsp25 levels remained relatively unchanged with aging, the Hsp70 level was increased in both brain and heart tissues of middle-aged rats. Chronic Sch B treatment was able to enhance mitochondrial antioxidant status and the resistance to Ca2+-induced mitochondrial permeability transition in an age-independent manner in various tissues of rats. However, Hsp25 and Hsp70 levels were only increased in young adult rats. The Sch B-induced enhancement of mitochondrial protective parameters in the heart was associated with the protection against myocardial ischemia-reperfusion injury in both young adult and middle-aged rats. The results suggest that chronic Sch B treatment may be beneficial for reversing the mitochondrial changes with aging and enhancing the heat shock response.