ABSTRACT
Aromatase is a key enzyme responsible for in vivo estrogen biosynthesis. Inhibition of the activity of the aromatase has become an alterative way for treatment of breast cancer. In this review, the structure and catalytic mechanism of the aromatase is briefly introduced followed by thorough review of the progress in the study of the steroidal and non-steroidal aromatase inhibitors. This review is focused on the natural compounds that exhibit the aromatase inhibition, which include flavonoids, xanthones, coumarins, and sesquiterpenes. The structure-activity relationship of these compounds is also discussed.
Subject(s)
Humans , Androstenedione , Antineoplastic Agents , Chemistry , Pharmacology , Therapeutic Uses , Aromatase , Chemistry , Metabolism , Pharmacology , Aromatase Inhibitors , Chemistry , Classification , Pharmacology , Therapeutic Uses , Breast Neoplasms , Drug Therapy , Catalysis , Coumarins , Chemistry , Pharmacology , Estrogens , Flavonoids , Chemistry , Pharmacology , Inhibitory Concentration 50 , Nitriles , Chemistry , Pharmacology , Sesquiterpenes , Chemistry , Pharmacology , Structure-Activity Relationship , Triazoles , Chemistry , Pharmacology , Xanthones , Chemistry , PharmacologyABSTRACT
<p><b>OBJECTIVE</b>To investigate the vascular activity of extract from mulberry leaves (EML) on rat thoracic aorta and the underlying mechanism.</p><p><b>METHODS</b>Isolated thoracic rings of Sprague-Dawley rats were mounted on the organ bath and the tension of the vessel was recorded.</p><p><b>RESULT</b>(1) EML produced a concentration-dependent vasorelaxation of aorta preconstricted by high K(+) (60 mmol/L) or 10(-6) mol/L phenylephrine (PE) in endothelium-intact and endothelium-denuded arteries. (2) EML at EC(50) concentration reduced the calcium dose-response curve. (3) After incubation of aorta with verapamil, EML induced vasocontraction of aorta preconstricted by PE, which was abolished by ruthenium red.</p><p><b>CONCLUSION</b>The vascular effect of EML is biphasic, the vasorelaxation is greater than the vasocontraction. The vasorelaxation induced by EML may be mediated by inhibition of voltage-and receptor-dependent calcium channels in vascular smooth muscle cells, while the vasocontraction is via activation of ryanodine receptor in endoplasmic reticulum.</p>