| First Author | Han Y | Year | 2021 |
| Journal | J Cell Mol Med | Volume | 25 |
| Issue | 18 | Pages | 8947-8956 |
| PubMed ID | 34405526 | Mgi Jnum | J:313024 |
| Mgi Id | MGI:6793529 | Doi | 10.1111/jcmm.16855 |
| Citation | Han Y, et al. (2021) Curcumin improves memory deficits by inhibiting HMGB1-RAGE/TLR4-NF-kappaB signalling pathway in APPswe/PS1dE9 transgenic mice hippocampus. J Cell Mol Med 25(18):8947-8956 |
| abstractText | Amyloid-beta (Abeta) deposition in the brain has been implicated in the development of Alzheimer's disease (AD), and neuroinflammation generates AD progression. Therapeutic effects of anti-inflammatory approaches in AD are still under investigation. Curcumin, a potent anti-inflammatory and antioxidant, has demonstrated therapeutic potential in AD models. However, curcumin's anti-inflammatory molecular mechanisms and its associated cognitive impairment mechanisms in AD remain unclear. The high-mobility group box-1 protein (HMGB1) participates in the regulation of neuroinflammation. Herein, we attempted to evaluate the anti-inflammatory effects of chronic oral administration of curcumin and HMGB1 expression in APP/PS1 transgenic mice AD model. We found that transgenic mice treated with a curcumin diet had shorter escape latencies and showed a significant increase in percent alternation, when compared with transgenic mice, in the Morris water maze and Y-maze tests. Additionally, curcumin treatment could effectively decrease HMGB1 protein expression, advanced glycosylation end product-specific receptor (RAGE), Toll-like receptors-4 (TLR4) and nuclear factor kappa B (NF-kappaB) in transgenic mice hippocampus. However, amyloid plaques detected with thioflavin-S staining in transgenic mice hippocampus were not affected by curcumin treatment. In contrast, curcumin significantly decreased GFAP-positive cells, as assessed by immunofluorescence staining. Taken together, these data indicate that oral administration of curcumin may be a promising agent to attenuate memory deterioration in AD mice, probably inhibiting the HMGB1-RAGE/TLR4-NF-kappaB inflammatory signalling pathway. |
