Abstract
Introduction:
Neuritic plaques, a neuropathologic hallmark of Alzheimer's disease, are extracellular deposits of β-amyloid peptides (Aβ). In the central nervous system neuritic plaques are surrounded by activated microglial cells expressing proinflammatory cytokines, chemokines, and neurotoxic mediators. Long-term activation of microglial cells is suspected to contribute to the neuron loss in Alzheimer's disease.
Objective:
This study was conducted to determine whether a ginger (Zingiber officinale and Alpinia galanga) extract (GE) can dampen the activation of THP-1 cells by lipopolysaccharide, proinflammatory cytokines, and fibrillar amyloid peptide Aβ(1-42), a major component of neuritic plaques.
Methods:
THP-1 cells, a human monocytic cell line with properties similar to human microglial cells, were incubated with GE or control medium alone for 1 hour, and then with reincubated lipopolysaccharide (LPS), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) or fibrillar Aβ(1-42) for an additional hour. The extent of THP-1 cell activation was determined by measuring mRNA levels of TNF-α and IL-1β, cyclooxygenase-2 (COX-2), macrophage inflammatory protein 1α (MIP-1α), monocyte chemoattractant protein-1 (MCP-1), and interferon-γ inducible protein 10 (IP-10).
Results:
The results document that the GE used in this study inhibits LPS, cytokine, and amyloid Aβ peptide- induced expression of the proinflammatory genes TNF-α, IL-1β, COX-2, MIP-α, MCP-1, and IP-10. The data provide experimental evidence that ginger can inhibit the activation of human monocytic THP-1 cells by different proinflammatory stimuli and reduce the expression of a wide range of inflammation-related genes in these microglial-like cells.
Conclusions:
The findings suggest that GE may be useful in delaying the onset and the progression of neurodegenerative disorders involving chronically activated microglial cells in the central nervous system.
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