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Role of nomilin in regulation of inflammatory pathways potentiated by Substance P and TNF‐alpha in cardiovascular cells
Author(s) -
Chakraborty Sanjukta,
Kim J.,
Jayaprakasha G.K,
Patil B.S.,
Muthuchamy M.
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.lb489
Subject(s) - umbilical vein , inflammation , p38 mitogen activated protein kinases , tumor necrosis factor alpha , limonoid , pharmacology , mapk/erk pathway , protein kinase a , signal transduction , pathogenesis , chemistry , microbiology and biotechnology , kinase , medicine , biology , endocrinology , biochemistry , botany , in vitro
Inflammation is the hallmark of cardiovascular disease (CVD) and several inflammatory pathways act in concert to contribute to its pathogenesis. Although several studies report an increase in fruit consumption reduces the risk of CVD, the specific mechanisms are poorly understood. We have previously purified and identified several limonoids from citrus fruits using novel chromatographic and spectroscopic techniques. In our present study, the effect was determined of one such citrus limonoid, nomilin, on the MAP kinase activity in cardiovascular cells. Human aortic smooth muscle cells (HASMCs), human umbilical vein endothelial cells (HUVECs) and rat lymphatic muscle cells (LMCs) were used. These cells were treated with nomilin at different concentrations followed by the treatment with either substance P (SP) or TNF‐alpha to activate MAPK pathway. Results demonstrate that nomilin completely reduced TNF‐alpha induced p38 MAP kinase activity in HASMCs. Furthermore, nomilin plays a significant role in the regulation of SP or TNF‐alpha mediated ERK1/2 and p38 MAP kinase activation in HUVECs and LMCs in a dose and time dependant manner. Taken together, we demonstrate for the first time that the citrus limonoid, nomilin, play a vital role in the modulation of pro‐inflammatory pathways in cardiovascular cells. Funding: USDA‐NIFA No. 2010‐34402‐20875 and “Designing Foods for Health,” VAFIC to BP, and NIH HL80526 and NIH KO2 HL86650 to MM.