PMID- 15673995
OWN - NLM
STAT- MEDLINE
DCOM- 20050519
LR  - 20240109
IS  - 1075-5535 (Print)
IS  - 1075-5535 (Linking)
VI  - 10
IP  - 6
DP  - 2004 Dec
TI  - Ginger extract inhibits beta-amyloid peptide-induced cytokine and chemokine 
      expression in cultured THP-1 monocytes.
PG  - 1009-13
AB  - INTRODUCTION: Neuritic plaques, a neuropathologic hallmark of Alzheimer's 
      disease, are extracellular deposits of beta-amyloid peptides (Abeta). 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 Abeta(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-alpha (TNF-alpha), interleukin-1beta (IL-1beta) or 
      fibrillar Abeta(1-42) for an additional hour. The extent of THP-1 cell activation 
      was determined by measuring mRNA levels of TNF-alpha and IL-1beta, 
      cyclooxygenase-2 (COX-2), macrophage inflammatory protein 1alpha (MIP-1alpha), 
      monocyte chemoattractant protein-1 (MCP-1), and interferon-gamma inducible 
      protein 10 (IP-10). RESULTS: The results document that the GE used in this study 
      inhibits LPS, cytokine, and amyloid Abeta peptide-induced expression of the 
      proinflammatory genes TNF-alpha, IL-1beta, COX-2, MIP-alpha, 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.
FAU - Grzanna, Reinhard
AU  - Grzanna R
AD  - RMG Biosciences, Inc., Baltimore, MD, USA.
FAU - Phan, Phong
AU  - Phan P
FAU - Polotsky, Anna
AU  - Polotsky A
FAU - Lindmark, Lars
AU  - Lindmark L
FAU - Frondoza, Carmelita G
AU  - Frondoza CG
LA  - eng
PT  - Journal Article
PL  - United States
TA  - J Altern Complement Med
JT  - Journal of alternative and complementary medicine (New York, N.Y.)
JID - 9508124
RN  - 0 (Amyloid beta-Peptides)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokine CCL3)
RN  - 0 (Chemokine CCL4)
RN  - 0 (Chemokine CXCL10)
RN  - 0 (Chemokines)
RN  - 0 (Chemokines, CXC)
RN  - 0 (Cytokines)
RN  - 0 (Interleukin-1)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Macrophage Inflammatory Proteins)
RN  - 0 (Membrane Proteins)
RN  - 0 (Peptide Fragments)
RN  - 0 (Plant Extracts)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0 (amyloid beta-protein (1-42))
RN  - EC 1.14.99.1 (Cyclooxygenase 2)
RN  - EC 1.14.99.1 (PTGS2 protein, human)
RN  - EC 1.14.99.1 (Prostaglandin-Endoperoxide Synthases)
SB  - IM
MH  - Alzheimer Disease/*drug therapy/metabolism
MH  - Amyloid beta-Peptides/*metabolism
MH  - Cell Culture Techniques
MH  - Chemokine CCL2/antagonists & inhibitors
MH  - Chemokine CCL3
MH  - Chemokine CCL4
MH  - Chemokine CXCL10
MH  - Chemokines/*antagonists & inhibitors
MH  - Chemokines, CXC/antagonists & inhibitors
MH  - Cyclooxygenase 2
MH  - Cytokines/*antagonists & inhibitors
MH  - Dose-Response Relationship, Drug
MH  - Gene Expression Regulation/drug effects
MH  - *Zingiber officinale
MH  - Humans
MH  - Interleukin-1/antagonists & inhibitors
MH  - Lipopolysaccharides/antagonists & inhibitors
MH  - Macrophage Inflammatory Proteins/antagonists & inhibitors
MH  - Membrane Proteins
MH  - Monocytes/*drug effects/metabolism
MH  - Peptide Fragments/*metabolism
MH  - Plant Extracts/pharmacology
MH  - Plaque, Amyloid/*drug effects/metabolism
MH  - Prostaglandin-Endoperoxide Synthases/drug effects
MH  - RNA, Messenger
MH  - Tumor Necrosis Factor-alpha/antagonists & inhibitors
EDAT- 2005/01/28 09:00
MHDA- 2005/05/20 09:00
CRDT- 2005/01/28 09:00
PHST- 2005/01/28 09:00 [pubmed]
PHST- 2005/05/20 09:00 [medline]
PHST- 2005/01/28 09:00 [entrez]
AID - 10.1089/acm.2004.10.1009 [doi]
PST - ppublish
SO  - J Altern Complement Med. 2004 Dec;10(6):1009-13. doi: 10.1089/acm.2004.10.1009.