Instituto Superior de Ciências Biomédicas, Universidade Estadual do Ceará, Fortaleza, Ceará, Brazil.
Fundam Clin Pharmacol. 2010 Jun;24(3):341-50. doi: 10.1111/j.1472-8206.2009.00768.x. Epub 2009 Aug 13.
Various essential oils are rich in carvacrol, a monoterpenic phenol isomeric with thymol. This study was undertaken to assess the vasorelaxant effects of thymol and carvacrol in rat isolated aorta and the putative mechanisms underlying these effects. Thymol and carvacrol produced a concentration-dependent relaxation on the aortic ring preparations pre-contracted using KCl (IC(50) value of 64.40 +/- 4.41 and 78.80 +/- 11.91 microm, respectively) or using phenylephrine (PHE, 0.1 microm) (IC(50) value of 106.40 +/- 11.37 and 145.40 +/- 6.07 microm, respectively) and inhibited the concentration-response curves of aortic rings to PHE or KCl. In Ca(2+)-free medium with ethylene glycol-bis(2-aminoethylether)-N,N,N',N'-tetraacetic acid (2 mm), thymol and carvacrol both at 1000 microm completely abolished the phasic component of PHE-induced endothelium-containing ring contractions. At 400 microm, thymol and carvacrol significantly reduced the CaCl(2)-induced contractions in Ca(2+)-free medium. Furthermore, both thymol and carvacrol (300 and 1000 microm) significantly reduced the contraction evoked by phorbol dibutyrate (1 microm), an activator of protein kinase C. Magnitude of this inhibitory effect was enhanced in the presence of the Ca2+ pump inhibitor, thapsigargin (1 microm). At 1000 microm, neither thymol nor carvacrol altered the resting potential of vascular smooth muscle cells. In conclusion, thymol and carvacrol induced an endothelium-independent relaxation in rat isolated aorta, an effect that seems mediated through some mechanisms probably involving a transduction pathway between Ca(2+) release from sarcoplasmic reticulum and/or regulation of the Ca2+ sensitivity of the contractile system. Moreover, it's conceivable that thymol and carvacrol, at low concentrations, block the Ca(2+) influx through the membrane.
各种精油富含香芹酚,这是与百里香酚同分异构的单萜酚。本研究旨在评估百里香酚和香芹酚对大鼠离体主动脉的血管舒张作用,以及这些作用的潜在机制。香芹酚和百里香酚对用 KCl(IC50 值分别为 64.40±4.41 和 78.80±11.91μM)或用苯肾上腺素(PHE,0.1μM)预收缩的主动脉环标本产生浓度依赖性舒张(IC50 值分别为 106.40±11.37 和 145.40±6.07μM),并抑制了主动脉环对 PHE 或 KCl 的浓度反应曲线。在含有乙二胺四乙酸(2mm)的无钙乙二醇双(2-氨基乙基醚)(EGTA)介质中,1000μM 的香芹酚和百里香酚均完全消除了 PHE 诱导的含内皮环收缩的相性成分。在 400μM 时,香芹酚和百里香酚显著降低了无钙介质中 CaCl2 诱导的收缩。此外,香芹酚和百里香酚(300 和 1000μM)显著降低了蛋白激酶 C 激活剂佛波醇二丁酸(1μM)引起的收缩。在存在钙泵抑制剂 thapsigargin(1μM)的情况下,这种抑制作用的幅度增强。在 1000μM 时,香芹酚和百里香酚均不改变血管平滑肌细胞的静息电位。总之,香芹酚和百里香酚诱导大鼠离体主动脉产生非内皮依赖性舒张,这种作用似乎通过一些机制介导,这些机制可能涉及肌浆网中 Ca2+释放和/或收缩系统 Ca2+敏感性的调节之间的转导途径。此外,可以设想,低浓度的香芹酚和百里香酚可以阻止通过膜的 Ca2+内流。