Lutein inhibits the function of TRPA1 but not TRPV1 in different in vitro and in vivo models
Éva
Szoke1*,
Ágnes
Kemény1,
Gyöngyi
Horváth2,
Péter
Molnár2,
József
Deli3,
Lajos
Szente4,
Tamás
Bozó5,
Szilárd
Pál5,
Attila
Dévay5,
Miklós
Simonyi6,
János
Szolcsányi1 and
Zsuzsanna
Helyes1
-
1
University of Pécs, Department of Pharmacology and Pharmacotherapy, Hungary
-
2
University of Pécs, Department of Pharmacognosy, Hungary
-
3
University of Pécs, Department of Biochemistry and Medical Chemistry, Hungary
-
4
Cyclolab Ltd., Hungary
-
5
University of Pécs, Department of Pharmacotechnology, Hungary
-
6
Hungarian Academy of Sciences, Chemical Research Center, Hungary
Transient Receptor Potential ion channels, such as TRP Vanilloid 1 and Ankyrin repeat domain 1 (TRPV1 and TRPA1), are expressed in primary sensory neurones. Their activation and the release of pro-inflammatory neuropeptides mediate neurogenic inflammation. We found that lutein, a natural tetraterpene carotenoid, inhibits neurogenic inflammation induced by TRPA1, but not TRPV1 activation, and that lipid rafts in the neural membrane are involved in TRPV1 functions. Since the structure of carotenoid suggests their ability to interfere with lipid rafts, the aim of these experiment was to investigate the mechanisms by which lutein modulates TRP channels and inhibits neurogenic inflammation.
The water-soluble random methyled β-cyclodextin (RAMEB) complex of lutein was studied on TRPV1 and TRPA1 activation on cell bodies and peripheral nerve terminals. Cultured rat trigeminal neurones and isolated trachea preparations were treated with the respective selective agonist, capsaicin (330 nM) or mustard oil (200 µM). [Ca2+]i was measured with microfluorimetry, calcitonin gene-related peptide (CGRP) release with radioimmunoassay. Capsaicin (2.5%) and mustard oil (3%)-induced neurogenic oedema and inflammatory cell accumulation in the mouse ear was determined with micrometry, histology and myeloperoxidase (MPO) measurement.
Mustard oil-induced Ca2+-influx in trigeminal sensory neurones and CGRP relesae from the nerve terminals were significantly inhibited by RAMEB-lutein (100 µM). Ear oedema and MPO activity indicating granulocyte accumulation were also diminished by RAMEB-lutein (100 µg/ml). In contrast, this carotenoid complex did not infuence capsaicin-evoked responses. These data demonstrate that lutein inhibits Ca2+ influx and CGRP release in vitro, as well as neurogenic inflammatory responses in vivo induced by TRPA1, but not TRPV1 stimulation. Based on these results and the structure of lutein, its ability to modulate lipid rafts in the membrane can be suggested.
Conference:
IBRO International Workshop 2010, Pécs, Hungary, 21 Jan - 23 Jan, 2010.
Presentation Type:
Poster Presentation
Topic:
Cellular neuroscience
Citation:
Szoke
É,
Kemény
Á,
Horváth
G,
Molnár
P,
Deli
J,
Szente
L,
Bozó
T,
Pál
S,
Dévay
A,
Simonyi
M,
Szolcsányi
J and
Helyes
Z
(2010). Lutein inhibits the function of TRPA1 but not TRPV1 in different in vitro and in vivo models.
Front. Neurosci.
Conference Abstract:
IBRO International Workshop 2010.
doi: 10.3389/conf.fnins.2010.10.00150
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Received:
29 Apr 2010;
Published Online:
29 Apr 2010.
*
Correspondence:
Éva Szoke, University of Pécs, Department of Pharmacology and Pharmacotherapy, Pécs, Hungary, eva.szoke@aok.pte.hu