Mitochondrial energy metabolism changes during aging-mouse cranial nerve cells treated with various doses and forms of Fructus schizandrae

摘要

BACKGROUND: During the cellular aging process, the number of mitochondria, generation of adenosine triphosphate (ATP), activity of respiratory chain enzyme complex 1 and 4, and oxidation decrease. OBJECTIVE: To observe the effects of aqueous and spirituous extract, as well as polysaccharides from Fructus schizandrae (Magnolia Vine) on energy metabolism and mitochondrial anti-oxidation in cranial nerve cells of a D-gal-induced aging mouse model. DESIGN, TIME AND SETTING: A randomized, controlled, animal study. The experiment was conducted at the Department of Biochemistry, Qiqihar Medical College between March and July 2006. MATERIALS: Fifty healthy, Kunming mice of both sexes, aged 2-3 months old and weighing 18-22 g, were used for the present study. Fructus schizandrae was purchased from the Medical College of Jiamusi University. Aqueous extracts, spirituous extracts, and polysaccharides from Fructus schizandrae were prepared. D-galactose (D-gal) is a product of the Second Reagent Factory, Shanghai City, China. Mn-superoxide dismutase (Mn-SOD) kit, malonaldehyde (MDA) kit, protein quantification kit, and inorganic phosphorus testing kit were purchased from Jian Cheng Bioeng. Co., China. METHODS: Fifty mice were randomly divided into five groups, with 10 mice in each group: young control, aging model, aqueous Fructus schizandrae extract, spirituous Fructus schizandrae extract, and Fructus schizandrae polysaccharides. Over a course of 30 days, mice in aging model, aqueous Fructus schizandrae extract, spirituous Fructus schizandrae extract, and Fructus schizandrae polysaccharides groups were injected subcutaneously with D-gal (100 mg/kg) into the nape of the neck daily, and administered intragastrically with an equal volume of sterile, warm water (aging model), aqueous Fructus schizandrae extract (2 g/kg), spirituous Fructus schizandrae extract (2 g/kg), or Fructus schizandrae polysaccharides (0.2 g/kg), respectively. Mice in the young control group were injected into the nape of the neck with physiological saline and administered intragastrically with sterile, warm water. MAIN OUTCOME MEASURES: Respiratory chain complex I and H+-ATP enzyme activities, as well as Mn-SOD and MDA levels, were determined by the Coomassie brilliant blue method. RESULTS: All fifty mice were included in the final analysis. In mitochondria from cranial nerve cells of the aging mouse group MDA levels were significantly increased, compared with young control group (P < 0.01); however, Mn-SOD levels, as well as respiratory chain complex I and H+-ATP enzyme activity, were remarkably decreased (P < 0.01). In each Fructus schizandrae group, Mn-SOD levels, as well as respiratory chain complex I and H+-ATP enzyme activity was enhanced to various extents (P < 0.05, P < 0.01), and MDA levels were decreased (P < 0.01), compared with the aging model group. CONCLUSION: Aqueous and spirituous Fructus schizandrae extracts, as well as Fructus schizandrae polysaccharides delayed changes in mitochondrial energy metabolism, increased Mn-SOD levels, and decreased MDA levels in cranial nerve cell mitochondria of an aging mouse model. Fructus schizandrae polysaccharides were particularly capable of protecting mitochondria from oxidative injury.