Effect of Rice Bran Antioxidant Peptides on Mitochondria Damage in Aging Mice Induced by D-galactose

Rice bran as raw material, the use of D-galactose (D-gal) induced aging mouse model study of antioxidant peptides from rice bran mitochondrial damage protection and its anti-aging effects, and to explore its mechanism of action. Kunming mice were randomly divided into young control group, the control group of aging, rice bran antioxidant peptides from low, medium and high dose treatment group, 12 in each group. Aging control group, rice bran antioxidant peptide treatment group daily subcutaneous injection of D-gal 100 mg / (kg-bw), young control group injected with normal saline; rice bran antioxidant peptide treatment group were administered daily rice bran anti- oxidized peptide of 100, 200, 500 mg / (kg-bw), the control group was given normal saline, continuous 6W; observed during the mice in each group signs performance weighed once a week. Liver cells was observed by transmission electron microscopy (TEM) and mitochondrial ultrastructure; ultraviolet spectrophotometry for the determination of the heart, brain, liver mitochondrial malondialdehyde (MDA) content, of manganese - superoxide dismutase (Mn-SOD ), glutathione peroxidase (GSH-Px), catalase (CAT) activity, total antioxidant capacity (T-AOC) and the heart, brain mitochondrial respiratory chain complex body I, II, Ⅴ activity; by polymerase chain reaction (PCR) technology and optical density scan to detect the impact of the peptide in mouse brain mitochondrial DNA (mtDNA) deletion mutations. The results are as follows: aging control mice liver mitochondrial swelling, vacuolization or deformity, reduce the number and disorganized, film and crest blurred even disappear, and rice bran antioxidant peptides from each group of mice mitochondria improvement in the degree of injury, the effect of 500 mg / (kg-bw). (2) Compared with the young control group, aging control mice heart, brain, liver mitochondrial Mn-SOD, GSH-Px, CAT activity, T-AOC vitality significantly reduced (P lt; 0.01), MDA content was significantly increased (P lt; 0.01), suggesting that D-gal can induce a large number of oxygen free radicals generated enhanced mitochondrial lipid peroxidation; compared with the control group of aging, rice bran antioxidant peptides from each group of mice a significant reduction in the mitochondrial content of MDA, antioxidant activity was significantly restored T-AOC vitality was significantly higher (P lt; 0.05), works best when the concentration of 500 mg / (kg bw). Show that rice bran antioxidant peptides through increased mitochondrial antioxidant capacity, remove excess free radicals, to inhibit the D-gal aging mice in mitochondrial lipid peroxidation injury. Compared with the young control group, aging control mice heart, brain mitochondrial respiratory chain complex I, II, Ⅴ activity decreased significantly (P lt; 0.01) the brain mtDNA deletion was significantly higher; aging control group compared to middle and high dose rice bran antioxidant peptides can significantly improve the aging mouse heart, brain mitochondrial respiratory chain complex I, II, the Ⅴ activity (P lt; 0.01 or P LT; 0.05), significantly reduced the brain mtDNA deletion mutations ( P lt; 0.01), 500 mg / (kg bw) dose optimal. The rice bran antioxidant peptide D-gal induced aging mice respiratory chain complex mtDNA has a good protection for its anti-aging at the molecular level possible. With the aging body increased free radical production, antioxidant enzyme activities decreased, resulting in the the mouse mitochondrial structure and function damage. Rice bran antioxidant peptide by scavenging free radicals, improve aging mice mitochondrial histologic features, Mn-SOD, GSH-Px, CAT, respiratory chain enzyme complexes I, II, Ⅴ activity and T-AOC activity and decreased MDA content and mtDNA deletion mutations, which play the role of aging.