RESUMO
Phytoestrogens exhibit various pharmacological estrogen-like effects, such as in the prevention and treatment of osteoporosis, cardiovascular diseases, tumors, etc., but the specific mechanism is still unclear. In recent years, estrogen receptor alpha-mediated rapid non-genomic effects have been identified to play an important role in the pathogenesis of estrogen-related diseases. The research of phytoestrogens exerting pharmacological effects through non-genomic effects has also received increasing attention. This article summarizes the research progress in estrogen receptor alpha-mediated non-genomic effects and analyzes the possible involvement of rapid non-genomic effects in certain pharmacological effects of phytoestrogens. The future prospects of estrogen receptor-mediated non-genomic effects by phytoestrogens are also discussed.
RESUMO
<p><b>OBJECTIVE</b>To reveal the nongenomic effect of aldosterone on the regulation of sodium intake in the nucleus tractus solitarius (NTS) and the role of central nucleus of the amygdala (CeA) in regulating this effect.</p><p><b>METHODS</b>Adult male SD rats were divided into four groups and underwent operations to induce bilateral CeA electrolytic lesions (400 μA, 25 s; =28), bilateral sham CeA lesions (=28), unilateral CeA lesions (=28), or unilateral sham CeA lesions (=26). After 3 days of recovery, the rats received implantation of a stainless steel 23-gauge cannula wih two tubes into the NTS followed by a recovery period of 7 days. The rats in each group were then divided into two subgroups for microinjection of aldosterone (50 ng/μL) or control solution in the NTS, and the cumulative intake within 30 min of 0.3 mol/L NaCl solution was recorded for each rat.</p><p><b>RESULTS</b>Bilateral CeA lesions (3 days) eliminated the increased 0.3 mol/L NaCl intake induced by aldosterone microinjected into the NTS (0.3±0.04 mL in CeA lesion group 1.3±0.3 mL in sham lesion group). Unilateral CeA lesion (3 days) reduced aldosterone-induced increase of NaCl intake in the first 15 min ( < 0.05) but not in 15-30 min ( > 0.05). In rats with sham lesions, aldosterone (50 ng/μL) still induced a significant increase in NaCl intake[1.3±0.3 mL 0.25±0.02 mL in the control group; F (3, 224)=24.0, < 0.05].</p><p><b>CONCLUSIONS</b>The regulation of sodium intake by aldosterone is subjected to descending facilitatory modulation by the bilateral CeA, and CeA integrity is essential for aldosterone to execute the nongenomic effect in regulating rapid sodium intake.</p>