Coeloglossum viride var. bracteatum extract improves cognitive deficits by restoring BDNF, FGF2 levels and suppressing RIP1/RIP3/MLKL-mediated neuroinflammation in a 5xFAD mouse model of Alzheimer's disease. (October 2021)

• Record Type: Journal Article
• Authors: Li, Xi-Xi; Cai, Zhe-Ping; Lang, Xiu-Yuan; Pan, Rui-Yuan; Ren, Teng-Teng; Lan, Rongfeng; Qin, Xiao-Yan
• Is Part Of: Journal of functional foods. Volume 85(2021)
• Publication Date: 2021-10
• Subjects: Aβ amyloid-β protein -- ALS amyotrophic lateral sclerosis -- AD Alzheimer's disease -- BDNF brain-derived neurotrophic factor -- CE Coeloglossum viride var. bracteatum extract -- FGF2 fibroblast growth factor 2 -- IL-6 interleukin-6 -- IL-1β interleukin-1β -- MWM Morris water maze -- MDA malondialdehyde -- MLKL Mixed lineage kinase domain-like protein -- SOD superoxide dismutase -- T-AOC total antioxidant capacity -- TBK1 TANK-binding kinase 1 -- RIP1 receptor-interacting serine/threonine-protein kinase 1 -- RIP3 receptor-interacting serine/threonine-protein kinase 3 -- GSH-Px glutathione peroxidase -- TNF-α tumor necrosis factor alpha; Aβ -- BDNF -- IBA1 -- Necroptosis -- TBK1 -- Y-maze test; Functional foods -- Analysis -- Periodicals; Food -- Biotechnology -- Periodicals; Nutrition -- Periodicals; 613.2
• DOI: 10.1016/j.jff.2021.104612
• Languages: English
• ISSNs: 1756-4646

Abstract

Graphical abstract: Highlights: CE restores cognitive deficits in 5xFAD mouse model of Alzheimer's disease. CE reduces Aβ plaques deposition in 5xFAD mice, consistent with their improved cognitive function. CE eliminates neuroinflammation and promotes neuronal survival by inhibiting the RIP1/RIP3/MLKL signaling pathway. Abstract: The neuroprotective effects of Coeloglossum viride var. bracteatum extract (CE) was investigated in a mouse model of AD. We found that CE improved cognitive deficits in 5xFAD mice in MWM and Y-maze behavioral tests. Also, antioxidant levels in serum and brain were normalized and peroxidation product MDA was reduced after CE treatment compared to untreated 5xFAD mice. Similarly, levels of pro-inflammatory factors such as TNF-α, IL-6 and IL-1β were reduced and anti-inflammatory factor IL-10 was increased. CE restored levels of BDNF and FGF2, as well as the signaling regulators Akt, TrkB and the apoptotic factors Bcl-2 and cleaved-Caspase-3. In addition, the RIP1/RIP3/MLKL inflammatory signaling pathway and necroptosis were inhibited, the RIP1 inhibitor TBK1 was restored and Aβ deposition was reduced in hippocampus and prefrontal cortex of 5xFAD mice. Thus, CE is effective in improving cognitive dysfunction in AD mouse models and may be a potential therapeutic agent.