Abstract: Objective: To investigate the regulatory effects of GPA on serum differential metabolites and elucidate the underlying mechanisms in D-Gal-induced aging mice. Method: The aging model was established through injection with D-Gal, and the administration group given GPA treatment simultaneously. The spatial cognition and memory ability was determined by Morris water maze test (MWM). Then detect mice serum antioxidant enzyme activity and lipid peroxide levels with the kit method. And Non-targeted metabolomics analysis of mice serum using UPLC-QTOF/MS. Results: Compared with the model group, GPA could shorten the escape latency of aging mice with various degrees, and the mice of GPA group spent significantly more time in the target quadrant. GPA (50 mg/kg) could increase mice serum activities of SOD (P<0.01), GSH-Px (P<0.01), and CAT (P<0.01) and reduce the level of MDA (P<0.01) in the serum of aging mice. In the serum of mice in the GPA group, 18 classes of differential metabolites were upregulated, and 6 classes were downregulated. . KEGG pathway enrichment analysis indicated that the differential metabolites were mainly enriched in inositol phosphate metabolism, steroid hormone biosynthesis, glutathione metabolism and primary bile acid biosynthesis metabolism pathways, etc. Conclusion: Oxidized glutathione, 18-hydroxycorticosterone, inositol-1,3,4,5-tetraphosphate, and D-inositol-1,4,5,6-tetraphosphate which may be important metabolites related to improve oxidative damage. This confirms that GPA could alleviate oxidative damage in aging mice, which may be related to enhancing the endogenous antioxidant system and the regulation of inositol phosphate metabolism, steroid hormone biosynthesis, glutathione metabolism and primary bile acid biosynthesis metabolism pathways, etc.