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Bromocriptine mesylate is an effective dopamine D2/D3 receptor agonist that binds to the dopamine D2 receptor with a pKi of 8.05 ± 0.2.
Related categories
Signal Pathways>>Autophagy>>Autophagy
Signal Pathways>>G Protein Coupled Receptors/G Proteins>>Dopamine Receptors
Signal Pathways>>Neural Signal Pathways>>Dopamine Receptors
Research Fields>>Neurological Diseases
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Target point
PKi: 8.05 ± 0.2 (dopamine D2 receiver) [1]
In vitro study of Bromocriptine stimulation [35S] - GTP γ S binds to D2 dopamine receptors expressed in CHO cells, with a pEC50 of 8.15 ± 0.05 [1]. Bromocriptine is also a strong inhibitor of brain nitric oxide synthase. Bromocriptine (BKT), an ergot alkaloid, has been found as a strong inhibitor of purified neuronal nitric oxide synthase (NOS) (IC50=10 ± 2) μ M) And it affects inducible macrophage NOS (IC50>100) μ M) The activity of [2] is very poor. Bromocriptine was found to inhibit the activity of at least one human cytochrome P450 enzyme. Bromocriptine is an effective CYP3A4 inhibitor with a calculated interaction IC50 value of 1.69 μ M [3].
In vivo studies were conducted in the forced swimming test (FST) and tail suspension test (TST), in which bleomycin mesylate (2mg/kg, ip) was administered for 7 days in the mouse group. Compared with the control group, the Bromocriptine group showed significant anti immobility effects. When bromocriptine was administered 30 minutes after the last 7-day MPE treatment and FST was performed, the dopamine agonist produced a significant and dose-dependent increase in the anti immobility effect of MPE (200mg/kg, oral) compared to MPE treatment alone. Compared with the control group, the Bromocriptine treatment group showed a significant reduction in immobility time. After pretreatment with MPE (100 and 200mg/kg, po) for 7 days, administration of bromocriptine showed a significant and dose-dependent enhancement of the anti immobility effect of MPE compared to MPE alone [4]. Compared with sham surgery (rats injected with saline), intraventricular administration of bromocriptine significantly reduced static mechanical abnormal pain (SMA) scores, and its effect persisted for 30 minutes. Compared with sham surgery, intraperitoneal administration of bromocriptine induced significant pain scores in the CCI-IoN group, with a dose-dependent decrease (0.1 mg and 1 mg/kg), and the effect persisted for 6 hours. The highest dose induction score showed the highest decrease (P<0.01). The Bromocriptine effect lasts for 20 minutes. Compared with sham surgery, intraperitoneal administration of bromocriptine induces SMA scores in the CCI-IoN+6-OHDA injury group