The regulatory effect of bromocriptine on cardiac hypertrophy by prolactin and D2 receptor modulation

Background Bromocriptine, a dopamine agonist, used for the treatment of hyperprolactinemia, type 2 diabetes, ovarian hyper-stimulation syndrome, has also effects on the cardiac remodeling process, but the mechanism of action is unknown. The aim of this work was to determinate the effect during hypertrophic process through molecular mechanisms that include prolactin receptor (Prlr) and receptor of dopamine 2 (D2 r) expression. Methods We used a model of cardiac hypertrophy induced by an aortocaval fistula (ACF) surgery in rats. Protein concentrations of D2 r and Prlr were determined by western blotting. The treatment consisted in water (control), captopril (50 mg/kg/day), bromocriptine (3 mg/kg/day), and ACF group (n = 6 per group). Results Our results showed that bromocriptine treatment decreases the hypertrophy index. Treatment with bromocriptine increases the protein expression of Prlr and D2 r in the cardiac tissue of rats with cardiac hypertrophy. Conclusions We concluded that bromocriptine has a protective effect on cardiac hypertrophy, and due to this effect, it may modulate the expression of Prlr and D2 r, which are involved in the development of cardiac hypertrophy

Glycine Effect on the Expression Profile of Orphan Receptors GPR21, GPR26, GPR39, GPR82 and GPR6 in a Model of Inflammation in 3T3-L1 Cells

Background: Chronic or low-grade inflammation is a process where various immune cells are recruited from the periphery into adipose tissue. This event gives rise to localised inflammation, in addition to having a close interaction with cardiometabolic pathologies where the mediation of orphan receptors is observed. The aim of this study was to analyse the participation of the orphan receptors GPR21, GPR39, GPR82 and GPR6 in a chronic inflammatory process in 3T3-L1 cells. The 3T3-L1 cells were stimulated with TNF-α (5 ng/mL) for 60 min as an inflammatory model. Gene expression was measured by RT-qPCR. Results: We showed that the inflammatory stimulus of TNF-α in adipocytes decreased the expression of the orphan receptors GPR21, GPR26, GPR39, GPR82 and GPR6, which are related to low-grade inflammation. Conclusions: Our results suggest that GPR21 and GPR82 are modulated by glycine, it shows a possible protective role in the presence of an inflammatory environment in adipocytes, and they could be a therapeutic target to decrease the inflammation in some diseases related to low-grade inflammation such as diabetes, obesity and metabolic syndrome