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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Sulforaphane improves oxidative status without attenuating the inflammatory response or cardiac impairment induced by ischemia-reperfusion in rats
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Sulforaphane improves oxidative status without attenuating the inflammatory response or cardiac impairment induced by ischemia-reperfusion in rats

机译：萝卜硫烷可改善氧化状态，而不会减弱大鼠缺血再灌注引起的炎症反应或心脏损害

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摘要

Sulforaphane, a natural isothiocyanate, demonstrates cardioprotection associated with its capacity to stimulate endogenous antioxidants and to inhibit inflammation. The aim of this study was to investigate whether sulforaphane is capable of attenuating oxidative stress and inflammatory responses through the TLR4/MyD88/NF kappa B pathway, and thereby could modulate post-ischemic ventricular function in isolated rat hearts submitted to ischemia and reperfusion. Male Wistar rats received sulforaphane (10 mg.kg(-1).day(-1)) or vehicle i.p. for 3 days. Global ischemia was performed using isolated hearts, 24 h after the last injection, by interruption of the perfusion flow. The protocol included a 20 min pre-ischemic period followed by 20 min of ischemia and a 20 min reperfusion. Although no changes in mechanical function were observed, sulforaphane induced a significant increase in superoxide dismutase and heme oxygenase-1 expression (both 66%) and significantly reduced reactive oxygen species levels (7%). No differences were observed for catalase and glutathione peroxidase expression or their activities, nor for thioredoxin reductase, glutaredoxin reductase and glutathione-S-transferase. No differences were found in lipid peroxidation or TLR4, MyD88, and NF-kappa B expression. In conclusion, although sulforaphane was able to stimulate endogenous antioxidants modestly, this result did not impact inflammatory signaling or cardiac function of hearts submitted to ischemia and reperfusion.
机译：萝卜硫素是一种天然的异硫氰酸酯，其心脏保护作用与其刺激内源性抗氧化剂和抑制炎症的能力有关。这项研究的目的是研究萝卜硫烷是否能够通过TLR4 / MyD88 / NF kappa B途径减轻氧化应激和炎症反应，从而能够调节缺血和再灌注的离体大鼠心脏的缺血后心室功能。雄性Wistar大鼠接受萝卜硫素（10 mg.kg（-1）.day（-1））或媒介物腹腔注射。 3天。在最后一次注射后24小时，通过中断灌注流，使用离体心脏进行整体缺血。方案包括缺血前20分钟，缺血20分钟和再灌注20分钟。尽管未观察到机械功能的变化，但萝卜硫烷诱导超氧化物歧化酶和血红素加氧酶-1的表达显着增加（均为66％），并显着降低了活性氧的水平（7％）。过氧化氢酶和谷胱甘肽过氧化物酶的表达或其活性，硫氧还蛋白还原酶，谷胱甘肽还原酶还原酶和谷胱甘肽-S-转移酶均未见差异。在脂质过氧化或TLR4，MyD88和NF-κB表达中未发现差异。总之，尽管萝卜硫烷能够适度地刺激内源性抗氧化剂，但该结果并未影响炎症和心肌缺血再灌注的心脏功能。

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