| First Author | Lee S | Year | 2024 |
| Journal | Chin Med | Volume | 19 |
| Issue | 1 | Pages | 95 |
| PubMed ID | 38965625 | Mgi Jnum | J:360733 |
| Mgi Id | MGI:7787279 | Doi | 10.1186/s13020-024-00966-2 |
| Citation | Lee S, et al. (2024) Rhei Undulati Rhizoma attenuates memory decline and reduces amyloid-beta induced neuritic dystrophy in 5xFAD mouse. Chin Med 19(1):95 |
| abstractText | BACKGROUND: Alzheimer's disease (AD) is a common type of dementia characterized by amyloid-beta (Abeta) accumulation, lysosomal dysfunction, and tau hyperphosphorylation, leading to neurite dystrophy and memory loss. This study aimed to investigate whether Rhei Undulati Rhizoma (RUR), which has been reported to have anti-neuroinflammatory effect, attenuates Abeta-induced memory impairment, neuritic dystrophy, and tau hyperphosphorylation, and to reveal its mode of action. METHODS: Five-month-old 5xFAD mice received RUR (50 mg/kg) orally for 2 months. The Y-maze test was used to assess working memory. After behavioral testing, brain tissue was analyzed using thioflavin S staining, western blotting, and immunofluorescence staining to investigate the mode of action of RUR. To confirm whether RUR directly reduces Abeta aggregation, a thioflavin T assay and dot blot were performed after incubating Abeta with RUR. RESULTS: RUR administration attenuated the Abeta-induced memory impairment in 5xFAD mice. Furthermore, decreased accumulation of Abeta was observed in the hippocampus of the RUR-treated 5xFAD group compare to the vehicle-treated 5xFAD group. Moreover, RUR reduced the dystrophic neurites (DNs) that accumulate impaired endolysosomal organelles around Abeta. In particular, RUR treatment downregulated the expression of beta-site amyloid precursor protein cleaving enzyme 1 and the hyperphosphorylation of tau within DNs. Additionally, RUR directly suppressed the aggregation of Abeta, and eliminated Abeta oligomers in vitro. CONCLUSIONS: This study showed that RUR could attenuate Abeta-induced pathology and directly regulate the aggregation of Abeta. These results suggest that RUR could be an efficient material for AD treatment through Abeta regulation. |
