Curcumin alleviates Alzheimer’s disease by inhibiting inflammatory response, oxidative stress and activating the AMPK pathway

• DOI: 10.1016/j.jchemneu.2023.102363
• Publication Date: 2023-11-19T15:21:12Z
• Authors: Sen Shao; Xiaojun Ye; Wenwen Su; Yanbo Wang
• Keywords: Nissl body; Terminal deoxynucleotidyl transferase; Malondialdehyde

Alzheimer's disease (AD) is a common degenerative brain disorder with limited therapeutic options. Curcumin (Cur) exhibits neuroprotective function in many diseases. We aimed to explore the role and mechanism of Cur AD. Firstly, we established AD mice by injecting amyloid-β1-42 (Aβ1–42) solution into hippocampus. Then, received 150 mg/kg/d for 10 consecutive days. The Morris water maze test was conducted evaluate cognitive hidden platform training probe trials. To assess spatial memory mice, spontaneous alternation behavior, number crossing novel arm time spent during Y-maze recorded. Hematoxylin eosin (H&E) staining terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNAL) assay were performed pathological damage apoptosis tissues. damaged neurons inspected Nissl staining. Immunohistochemical then detect Aβ1-42 deposition. levels tumor necrosis factor-α (TNF-a), interleukin-6 (IL-6) interleukin-1β (IL-1β) serum hippocampus, contents super oxide dismutase (SOD) malondialdehyde (MDA) tissues assessed enzyme-linked immunosorbent (ELISA). Additionally, B-cell lymphoma-2 (Bcl-2), Bcl-2 associated X protein (Bax), RelA (p65) expressions Adenosine 5'-monophosphate-activated kinase (AMPK) phosphorylation tested using Western blot. not only improved memory, but also alleviated mice. Meanwhile, upon treatment, decreased, level significantly decreased. Furthermore, treated exhibited lower TNF-a, IL-6, IL-1β MDA higher SOD content. Besides, downregulated p65 expression upregulated AMPK phosphorylation. may improve via suppressing inflammatory response, oxidative stress activating pathway, suggesting that be potential drug