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首页> 外文期刊>Digestive Diseases and Sciences >Ursodeoxycholic Acid and In Vitro Vasoactivity of Hydrophobic Bile Acids
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Ursodeoxycholic Acid and In Vitro Vasoactivity of Hydrophobic Bile Acids

机译：熊去氧胆酸和疏水性胆汁酸的体外血管活性

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Lipophilic bile acids, such as deoxycholic acid (DCA), are nonspecific endothelium-independent vasorelaxants whose underlying basis is complex, involving membrane calcium channels blockade and receptor antagonism. The vasorelaxant action of these acids has also been linked to the generation of reactive oxygen species and an increased extent of lipid peroxidation. Ursodeoxycholic acid (UDCA) is a naturally occurring tertiary dihydroxy hydrophilic acid whose mechanism of action has been attributed to minimizing the effects of lipophilic bile acids. Hence, we considered UDCA might be a useful pharmacological tool to delineate the role of enhanced lipid peroxidation in lipophilic bile acid-induced vasorelaxation. UDCA abrogates in vitro DCA-induced vasorelaxation in rat aortic rings and can suppress DCA-initiated lipid peroxidation in vascular smooth muscle microsomal membrane fractions prepared from the rat aortae. Three different studies were performed. In study 1, the ability of UDCA to restore the DCA-blunted contractile response to the α1-adrenoceptor, phenylephrine in rat aortic rings, was evaluated. In study 2, the ability of UDCA to restore DCA-induced vasorelaxation in precontracted rat aortic rings was assessed. In study 3, the ability of UDCA to suppress the increased extent of lipid peroxidation effected by DCA in vascular smooth muscle microsomal membrane fractions prepared from rat aortae was measured using the thiobarbituric acid reactive substance (TBARS) assay. UDCA, at a concentration equivalent to that seen in the plasma of patients with cholestatic liver disease treated with the bile acid, partially restored DCA-induced impaired contractility, prevented DCA-induced vasorelaxation, and abolished DCA-induced increases in the extent of lipid peroxidation. In conclusion, these data suggest that DCA-induced vasorelaxation is mediated by increasing the extent of lipid peroxidation in vascular tissue.
机译：亲脂性胆汁酸，例如脱氧胆酸（DCA），是非特异性内皮依赖性血管舒张剂，其基础很复杂，涉及膜钙通道阻滞和受体拮抗作用。这些酸的血管舒张作用也与活性氧的产生和脂质过氧化程度的增加有关。熊去氧胆酸（UDCA）是天然存在的叔二羟基亲水酸，其作用机理归因于使亲脂性胆汁酸的作用最小化。因此，我们认为UDCA可能是一种有用的药理学工具，可以描述增强的脂质过氧化作用在亲脂性胆汁酸诱导的血管舒张中的作用。 UDCA消除了大鼠主动脉环中体外DCA诱导的血管舒张，并可以抑制由大鼠主动脉制备的血管平滑肌微粒体膜级分中DCA引发的脂质过氧化。进行了三个不同的研究。在研究1中，评估了UDCA恢复DCA钝化大鼠主动脉环中对α1肾上腺素受体，去氧肾上腺素的收缩反应的能力。在研究2中，评估了UDCA恢复预收缩大鼠主动脉环中DCA诱导的血管舒张的能力。在研究3中，使用硫代巴比妥酸反应性物质（TBARS）测定了UDCA抑制DCA影响的由大鼠主动脉制备的血管平滑肌微粒体膜级分中脂质过氧化程度增加的能力。 UDCA的浓度等于胆汁酸治疗胆汁淤积性肝病患者血浆中的浓度，可部分恢复DCA引起的收缩力受损，防止DCA引起的血管舒张，并消除DCA引起的脂质过氧化程度的增加。总之，这些数据表明DCA诱导的血管舒张作用是通过增加血管组织中脂质过氧化的程度来介导的。

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