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Alleviative Effects of Ellagic Acid and Ursolic Acid on the Induction of Aging by Dietary AGE

Abstracts


Accumulation of dietary sources of advanced glycation end products (AGEs) are observed in the aging population and AGEs consequently increased oxidative stress, which can directly affect the function of different tissues and organs. D-galactose is a common reducing sugar and, at high levels, can induce oxidative stress in vivo to mimic the natural aging process in mice and rats. Both were used in the present study of ellagic acid and ursolic acid as defence agents against glycation and glycationmediated aging. Mitochondrial DNA (MtDNA) common deletion, the oxidative stress and inflammatory status are used as biomarkers of aging. The results of this study will be helpful for us to understand the process and prevention of aging. In this study, mice administration with D-gal result inflammation and MtDNA depletion in brain. But mice administration with D-gal and AGE result inflammation, oxidation in brain and liver, increasing of serum fructosamine and MtDNA depletion in brain. Treatments with 50 mg/kg AG (positive control), 25 mg/kg EA or 5 mg/kg UA in D-gal+AGE administration mice decrease levels of inflammation and MtDNA depletion in brain. Treatments with 50 mg/kg EA or 10 mg/kg UA in D-gal+AGE administration mice would decrease levels of inflammation, oxidation in brain and liver, increasing of serum fructosamine and MtDNA depletion in brain. Taken together, 50 mg/kg EA or 10 mg/kg UA attenuate D-gal and AGE result inflammation, oxidation in brain and liver, increasing of serum fructosamine and MtDNA depletion in brain.

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