Article Sidebar
Published:
Oct 5, 2016Keywords:
Article Details
Submission of a manuscript to this journal is a representation that the manuscript has not been published previously and is not under consideration for publication elsewhere.
All authors named in each manuscript would be required to sign a form (to be supplied by the Editor) so that they may retain their copyright in the article but to assign to us (the Publishers) and its licensees in perpetuity, in all forms, formats and media (whether known or created in the future) to (i) publish, reproduce, distribute, display and store the contribution, (ii) translate the contribution into other languages, create adaptations, reprints, include within collections and create summaries, extracts and/or abstracts of the contribution, (iii) create any other derivative works(s) based on the contribution, (iv) to exploit all subsidiary rights in the contribution, (v) the inclusion of electronic links from the contribution to third party material where-ever it may be located, and (vi) license any thrid party to do any or all of the above.
Main Article Content
Anti-hyperprolactinemia mechanism of Radix bupleuri extract in rats
Abstract
Purpose: To determine the mechanism underlying the anti-hyperprolactinemia effects of Radix bupleuri extract (RBE) in rats.
Methods: Rats were divided into six groups (n=10 each group): healthy controls, untreated hyperprolactinemic rats, hyperprolactinemic rats treated with bromocriptine (0.6 mg/kg), and hyperprolactinemic rats treated with RBE (4.8, 9.6, or 19.2 g/kg). After 30 days, hypothalamic protein levels of dopamine D2 receptor, protein kinase A (PKA), and cyclic adenosine monophosphate (cAMP) were determined.
Results: Dopamine D2 receptor levels were lower in untreated hyperprolactinemic rats than in healthy controls (p < 0.01), but this decrease was attenuated by RBE (p < 0.05). Elevated PKA levels in untreated hyperprolactinemic rats (0.61 ± 0.04 μg/ml, p < 0.01) were decreased by RBE (4.8 g/kg, 0.42 ± 0.03 μg/ml, p < 0.05; 9.6 g/kg, 0.33 ± 0.02 μg/ml, p < 0.01; 19.2 g/kg, 0.27 ± 0.03 μg/ml, p < 0.01). Similarly, elevated cAMP levels in hyperprolactinemic rats (2.4 ± 0.4 ng/ml) were decreased by RBE (4.8 g/kg, 1.8 ± 0.3 ng/ml, p < 0.05; 9.6 g/kg, 1.5 ± 0.3 ng/ml, p < 0.01; 19.2 g/kg, 1.2 ± 0.2 ng/ml, p < 0.01).
Conclusions: RBE anti-hyperprolactinemia activity is mediated by dopamine D2 receptor signaling via the cAMP/PKA pathway.
Keywords: Hyperprolactinemia, Radix bupleuri, Dopamine D2 receptor, cAMP/PKA
