The Inhibition of Mitogen-Activated Protein Kinases (MAPKs) and NF-κB Underlies the Neuroprotective Capacity of a Cinnamon/Curcumin/Turmeric Spice Blend in Aβ-Exposed THP-1 Cells.
Alessandro MaugeriCaterina RussoGiuseppe Tancredi PatanèDavide BarrecaGiuseppina MandalariMichele NavarraPublished in: Molecules (Basel, Switzerland) (2023)
Alzheimer's disease (AD) is a neurodegenerative disorder characterized by an increased level of β-amyloid (Aβ) protein deposition in the brain, yet the exact etiology remains elusive. Nowadays, treatments only target symptoms, thus the search for novel strategies is constantly stimulated, and looking to natural substances from the plant kingdom. The aim of this study was to investigate the neuroprotective effects of a spice blend composed of cinnamon bark and two different turmeric root extracts (CCSB) in Aβ-exposed THP-1 cells as a model of neuroinflammation. In abiotic assays, CCSB demonstrated an antioxidant capacity up to three times stronger than Trolox in the ORAC assay, and it reduced reactive oxygen species (ROS) induced by the amyloid fragment in THP-1 cells by up to 39.7%. Moreover, CCSB lowered the Aβ stimulated secretion of the pro-inflammatory cytokines IL-1β and IL-6 by up to 24.9% and 43.4%, respectively, along with their gene expression by up to 25.2% and 43.1%, respectively. The mechanism involved the mitogen-activated protein kinases ERK, JNK and p38, whose phosphorylation was reduced by up to 51.5%, 73.7%, and 58.2%, respectively. In addition, phosphorylation of p65, one of the five components forming NF-κB, was reduced by up to 86.1%. Our results suggest that CCSB can counteract the neuroinflammatory stimulus induced by Aβ-exposure in THP-1 cells, and therefore can be considered a potential candidate for AD management.
Keyphrases
- induced apoptosis
- signaling pathway
- cell cycle arrest
- gene expression
- pi k akt
- reactive oxygen species
- cell death
- oxidative stress
- endoplasmic reticulum stress
- cell proliferation
- traumatic brain injury
- high throughput
- lps induced
- multiple sclerosis
- physical activity
- dna methylation
- cerebral ischemia
- immune response
- inflammatory response
- climate change
- binding protein
- subarachnoid hemorrhage
- anti inflammatory