Cabergoline functions as a potent agonist of D2, D3, and 5-HT2B receptors. Pre-exposure to Cabergoline inhibits hydrogen peroxide (H2O2)-induced neuronal cell death in a dose-dependent manner. In the subsequent experiments, a concentration of 10 μM of Cabergoline is employed to explore its neuroprotective effects. Immunostaining for microtubule-associated protein 2 (MAP2) demonstrates that Cabergoline significantly attenuates the neuronal loss induced by H2O2 incubation. The observation of condensed apoptotic nuclei suggests that Cabergoline mitigates apoptotic cell death subsequent to exposure to H2O2.
Cabergoline/卡麦角林 动物研究
Animal study
The most notable decrease in rapid eye movement (REM) sleep episode count occurs during the light phase, wherein female mice administered with Cabergoline exhibit a reduction of 67.3% in REM sleep episodes (F(1,11)=12.892, P=0.004). Although the most substantial reduction in REM sleep episodes occurs during the dark phase (82.3% fewer REM sleep episodes; F(1,11)=3.667, P=0.082). In male mice, Cabergoline lowers baseline levels of prolactin (PRL) by 98.5% (F(1,6)=13.192, P=0.011), decreasing from 5.8±1.3 to 0.08 ng/mL within 2 hours post-injection. Following a 7-day recovery period, PRL levels revert to values that are statistically indistinguishable from baseline (5.0±0.60 ng/mL; F(1,6)=0.715, P=0.43).
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