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Article Publish Status: FREE
Abstract Title:

Astragaloside IV prevents memory impairment in D-galactose-induced aging rats via the AGEs/RAGE/ NF-κB axis.

Abstract Source:

Arch Med Res. 2021 Jul 1. Epub 2021 Jul 1. PMID: 34217517

Abstract Author(s):

Wei Li, Shuo Wang, Hao Wang, Jiepeng Wang, Feng Jin, Fang Fang, Chaoyi Fang

Article Affiliation:

Wei Li

Abstract:

BACKGROUND: We investigated the effects of astragaloside IV (AS-IV) on memory function in aging rats mimicked by D-galactose administration and explored the potential molecular mechanisms.

METHODS: Twenty-seven male rats were randomly divided into control group (N = 9), model group (N = 9), and AS-IV treated group (N = 9). Aging model was stimulated by D-galactose (400 mg/kg/d, i.p., dissolved in saline) for 8 weeks in rats. The general status of the rats was observed weekly. Learning and memory function was determined using the eight-arm radical mazeand step-down test. Pathological changes in the hippocampal CA1 region were determined by hematoxylin and eosin staining. Organ indexes, superoxide dismutase (SOD) activity and malonaldehyde (MDA) content in the serum were measured. Expression of advanced glycation end products (AGEs), receptor forAGEs (RAGE), nuclear factor-κB (NF-κB), interleukin (IL)-6, IL-1β and tumor necrosis factor-α (TNF-α) were detected by enzyme-linked immunosorbent assay, real-time polymerase chain reaction or western blotting.

RESULTS: AS-IV improved the general status of the aging rats induced by D-galactose, prevented the impairment of memory function, organ indexes, and the pathological damage of the hippocampus. From the prospective of oxidative stress, AS-IV increased sera SOD activity and decreased MDA content. Additionally, AS-IV also reduced the inflammatory response by reducing hippocampal IL-1β, TNF-α, and IL-6 expression. Importantly, AS-IV prevented D-galactose-induced expression of AGEs, RAGE and NF-κB in the hippocampus.

CONCLUSION: AS-IV could prevent D-galactose-induced aging and memory impairment in rats, likely via regulation of inflammatory response, which was modulated by AGEs/RAGE/NF-κB axis.

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