Diverse effects of taurine on vascular response and inflammation in GSH depletion model in rabbits.
OBJECTIVE
A reduction in GSH and an increase in free radicals are observed in inflammatory diseases, indicating oxidative stress. Taurine protects cells from the cytotoxic effects of inflammation. There have been limited studies to date evaluating the effect of taurine in oxidative stress-induced vascular dysfunction and its role in vascular inflammatory diseases. Therefore, we aimed to investigate the effect of taurine on the regulation of vascular tonus and vascular inflammatory markers in rabbit aortae and carotid arteries in oxidative stress-induced by GSH depletion.


METHODS
Rabbits were treated subcutaneously with buthionine sulfoximine (BSO), GSH-depleting compound and/or taurine. Cumulative concentration-response curves for acetylcholine (ACh), phenylephrine and 5-hydroxytriptamine (5-HT) were constructed with or without Nω-nitro-L-arginine (LNA) in the carotid artery and aorta rings. Immunohistochemical staining was performed for TNF-α and IL-1β.


RESULTS
BSO increased ACh-induced NO-dependent relaxations, phenylephrine-induced contractions in the carotid artery and 5-HT induced-contractions in both the carotid artery and the aorta. BSO decreased EDHF dependent relaxations only in the aorta. ACh-induced NO-dependent relaxations and augmented contractions were normalized by taurine. BSO increased TNF-α expressions in both carotid arteries and aortas, which were reversed by taurine. The BSO-induced increase in IL-1β was reversed by taurine only in aortae.


CONCLUSIONS
Treatment with BSO resulted in vascular reactivity changes and increased immunostaining of TNF-α in mainly carotid arteries in this model of oxidative stress. The effect of taurine on BSO-induced vascular reactivity changes varied depending on the vessel. The inhibition of the increase in TNF-α expression by taurine in both carotid arteries and aortae supports the proposal that taurine has a beneficial effect in the treatment of inflammatory diseases such as atherosclerosis.
Department of Pharmacology, Faculty of Pharmacy, Ege University, Bornova, Izmir, Turkey. gonen.ozsarlak@ege.edu.tr.
G
G
Ozsarlak-Sozer
G
G
Sevin
H H
HH
Ozgur
G
G
Yetik-Anacak
Z
Z
Kerry
D000109:Acetylcholine / Q000378:metabolism; D000818:Animals; D001011:Aorta / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D019328:Buthionine Sulfoximine / Q000494:pharmacology; D002339:Carotid Arteries / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D005978:Glutathione / Q000032:analysis / Q000378:metabolism*; D007150:Immunohistochemistry; D007249:Inflammation; D053583:Interleukin-1beta / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000032:analysis; D009569:Nitric Oxide / Q000378:metabolism; D019335:Nitroarginine / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects; D011817:Rabbits; D013654:Taurine / Q000494:pharmacology*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D053583:Interleukin-1beta; D014409:Tumor Necrosis Factor-alpha; D013654:Taurine; D019335:Nitroarginine; D009569:Nitric Oxide; D008315:Malondialdehyde; D019328:Buthionine Sulfoximine; D005978:Glutathione; D000109:Acetylcholine