Premium
The beneficial effect of clove essential oil and its major component, eugenol, on erectile function in diabetic rats
Author(s) -
YilmazOral Didem,
Onder Alev,
Gur Serap,
CarbonellBarrachina Ángel A.,
KayaSezginer Ecem,
Oztekin Cetin Volkan,
Zor Murat
Publication year - 2020
Publication title -
andrologia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.633
H-Index - 59
eISSN - 1439-0272
pISSN - 0303-4569
DOI - 10.1111/and.13606
Subject(s) - glibenclamide , formononetin , erectile dysfunction , nitric oxide , diabetes mellitus , pharmacology , medicine , endocrinology , cgmp specific phosphodiesterase type 5 , eugenol , nitric oxide synthase , chemistry , genistein , daidzein , organic chemistry
Abstract Diabetic men are at a higher risk of erectile dysfunction (ED). A tropical plant, clove (Syn. Eugenia caryophyllata , Caryophyllus aromaticus L., Syzygium aromaticum (L.) Merr. & L.M. Perry) from the Myrtaceae family has displayed aphrodisiac activity. The present research aimed to investigate the impacts of clove essential oil (CEO) and the ingredient of CEO, eugenol (E) on ED in diabetic rats. We divided Sprague‐Dawley rats into control and diabetic groups. Erectile function was evaluated before and after CEO and E intracavernosal injection. CEO‐ and E‐induced relaxation responses were investigated in isolated corpus cavernosum (CC) using various inhibitors. The intracavernous administration of CEO and E restored erectile responses in diabetic rats. CEO and E induced remarkable relaxation in all groups. CEO‐ and E‐induced relaxation responses were partially inhibited after pre‐contraction with KCl. Tetraethylammonium and glibenclamide inhibited the relaxation response to CEO. Glibenclamide inhibited maximum relaxation to E. The inhibitors of nitric oxide synthase (NOS), soluble guanylyl cyclase and nifedipine did not change CEO‐ and E‐induced relaxation responses. The current results suggest that CEO and the major compound of the essential oil, E improved diabetes‐induced ED in rats, and CEO caused CC relaxation via K + channels independently NO signalling pathway.