Ozsarlak-Sozer G, Sevin G, Ozgur H H, Yetik-Anacak G, Kerry Z
Department of Pharmacology, Faculty of Pharmacy, Ege University, Bornova, Izmir, Turkey.
Eur Rev Med Pharmacol Sci. 2016 Apr;20(7):1360-72.
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.
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.
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.
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.
在炎症性疾病中观察到谷胱甘肽(GSH)减少和自由基增加,提示存在氧化应激。牛磺酸可保护细胞免受炎症的细胞毒性作用。迄今为止,评估牛磺酸对氧化应激诱导的血管功能障碍的影响及其在血管炎性疾病中的作用的研究有限。因此,我们旨在研究牛磺酸对谷胱甘肽耗竭诱导的氧化应激状态下兔主动脉和颈动脉血管张力调节及血管炎症标志物的影响。
家兔皮下注射丁硫氨酸亚砜胺(BSO,一种GSH耗竭化合物)和/或牛磺酸。在有或无Nω-硝基-L-精氨酸(LNA)存在的情况下,构建颈动脉和主动脉环对乙酰胆碱(ACh), 去氧肾上腺素和5-羟色胺(5-HT)的累积浓度-反应曲线。对肿瘤坏死因子-α(TNF-α)和白细胞介素-1β(IL-1β)进行免疫组织化学染色。
BSO增加了ACh诱导的颈动脉中依赖一氧化氮(NO)的舒张、去氧肾上腺素诱导的颈动脉收缩以及5-HT诱导的颈动脉和主动脉收缩。BSO仅降低了主动脉中依赖内皮衍生超极化因子(EDHF)的舒张。牛磺酸使ACh诱导的依赖NO的舒张和增强的收缩恢复正常。BSO增加了颈动脉和主动脉中TNF-α的表达,而牛磺酸可使其逆转。BSO诱导的IL-1β增加仅在主动脉中被牛磺酸逆转。
在该氧化应激模型中,用BSO处理导致血管反应性改变,并主要在颈动脉中增加TNF-α的免疫染色。牛磺酸对BSO诱导的血管反应性变化的影响因血管而异。牛磺酸对颈动脉和主动脉中TNF-α表达增加的抑制作用支持了牛磺酸在治疗动脉粥样硬化等炎性疾病中具有有益作用的观点。