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.
ASJC Scopus subject areas
- Complementary and alternative medicine