| Abstract: |
The present disclosure
is directed to methods of determination of cellular targets
of herbal extracts. While much of this discussion is directed
to feverfew, the methods and process are applicable to other
extracts as well, and in one particular embodiment, to other
herbal extracts.
The herb feverfew is a folk remedy for various symptoms including
inflammation. Inflammation has recently been implicated in the
genesis of many diseases including cancers, atherosclerosis,
and rheumatoid arthritis. The mechanisms of action of feverfew
in the human body are largely unknown. To determine the cellular
targets of feverfew extracts, oligo microarrays have been utilized
to study the gene expression profiles elicited by feverfew extracts
in human monocytic THP-1 cells. 400 genese have been identified
that are consistently regulated by feverfew extracts. Most of
the genes are involved in cellular metabolism. However, the
genes undergoing the highest degree of change by feverfew treatments
are involved in other pathways including cheokine function,
water homeostasis, and heme-mediated signaling. Our results
also suggest that feverfew extracts suppress LPS-mediated TNF-a
and CCL@ (MCP-1) releases by THP-1 cells. It is hypothesized
that feverfew extracts components inhibit inflammatory cytokine
functions in human monocytes/macrophages.
Three feverfew extracts (SFE, SRE, and DeWE) have been prepared
using different extraction methods to test the hypothesis that
certain extraction methods can produce more active ingredients
with anti-migraine activity than others. Utilizing microarray
to profile the gene expression in human THP-1 monocytes, our
results suggests that SFE and SRE affect many more genes than
DeWE does. We have identified 198 genes in human macrophages
that are responding to SRE and SFE but not to DeWE (presumptive
inactive) and 10 selected genes were confirmed by RT-PCR. We
hypothesize that AQP-1, CCL2, and HMOX-1 may represent major
targets of feverfew functions. To address the functional roles
of feverfew extracts in the inflammatory pathways, we assayed
the effects of feverfew extracts on LPS-mediated cytokine releases
of human THP-1 monocytes. Our results suggest that feverfew
extracts strongly suppressed LPS-mediated productions of both
TNF-alpha and CCL2 (MCP-1). We utilized network analysis and
identified new candidate pathways as functional targets of feverfew
extracts in human monocytes.
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| Patent Status: |
Patent application has been filed. Detailed
information must be provided under a confidential disclosure agreement.
Please download the confidential disclosure form and mail the
completed form to:
Vincie Albritton, Associate Director
Clemson Research Park
Office of Technology Transfer
91 Technology Drive
A.M.R.L. Building, Room # 220
Anderson, SC 29625
|
| Contact: |
For more information about this
technology, please contact:
Vincie Albritton, Associate Director
Phone: (864) 656-5708
Fax: (864) 656-0474
email: valbrit@clemson.edu
or
Janet Dillon, Project Administrator
Phone: (864) 656-4237
Fax: (864) 656-0474
email: gjanet@clemson.edu
Note: Don't forget to include the technology number in
your emails!
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