Journal
ANTIOXIDANTS
Volume 10, Issue 11, Pages -Publisher
MDPI
DOI: 10.3390/antiox10111792
Keywords
ibogaine; K-ATP channels; glibenclamide; beta-adrenergic receptors; propranolol; antioxidative enzymes; superoxide dismutase; catalase; uterus; contractility
Funding
- Ministry of Education, Science and Technological Development of the Republic of Serbia [451-03-68/2020-14/200007]
- Slovenian ARRS Programme [P3-0171]
- Institute for Biological Research Sinisa StankovicNational Institute of Republic of Serbia, University of Belgrade
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The effects of ibogaine on the uterus are mediated by cellular receptors, ATP depletion, ROS production, and elevation of antioxidant enzyme activity. The study showed that ibogaine increased spontaneous activity in the uterus, and this effect was mediated by beta-adrenergic receptors and K-ATP channels. The pro-antioxidant effectiveness of ibogaine is linked to these cellular mechanisms.
Ibogaine effects are mediated by cellular receptors, ATP depletion followed by ROS production and antioxidant enzyme activity elevation in a dose and time dependent manner. Since the role of K-ATP channels and beta-adrenoceptors in ROS cellular circuit was established here we explored their role in ibogaine pro-antioxidant effectiveness. Single dose of ibogaine (10 mg/L i.e., 28.8 mu mol/L) was applied to isolated rat uterus (spontaneous and Ca2+-stimulated) and contractility and antioxidant enzymes activity were monitored during 4 h. Ibogaine increased amplitude and frequency of spontaneous active uteri immediately after addition that was prevented by propranolol (beta(1) and beta(2) adrenoceptors selective antagonists) and glibenclamide (K-ATP sensitive channels inhibitor; only frequency) pre-treatment. In Ca2+-stimulated uteri, ibogaine decreased both amplitude and frequency after 4 h. Pre-treatment with propranolol abolished ibogaine induced amplitude lowering, while glibenclamide had no effect. In both types of active uterus, ibogaine induced a decrease in SOD1 and an increase in CAT activity after 2 h. In Ca2+-stimulated uterus, there was also a decrease of SOD2 activity after 2 h. After 4 h, SOD1 activity returned to the baseline level, but GSH-Px activity increased. Pre-treatment with both propranolol and glibenclamide abolished observed changes of antioxidant enzymes activity suggesting that ibogaine pro-antioxidative effectiveness is beta-adrenergic receptors and K-ATP channels mediated.
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