Quetiapine is a 5-HT receptors agonist with a pEC50 of 4.77 for human 5-HT1A receptor. Quetiapine is a dopamine receptor antagonist with a pIC50 of 6.33 for human D2 receptor. Quetiapine is an atypical antipsychotic used to treat schizophrenia, bipolar disorder, and major depressive disorder[1].
Quetiapine (1, 10μM; 48h) causes cell cycle exit and promotes cell differentiation in primary oligodendrocyte cultures[2].Quetiapine (10, 20, 50μg/mL; 12h) treated had significantly lower levels of MDA and significantly higher activities of SOD and GSH-Px[3].Quetiapine (<100μM; 24h) has no significant effect on cell viabilities[4].
Quetiapine (400 mg/mL; surface application; 0, 6, 12, 24h) treatment significantly reduced skin thickening, erythema and edema, and inflammation caused by UVB irritation. In addition, Quetiapine treatment increased the activity of antioxidant enzymes, including superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), while reducing the production of the oxidised lipid malondialdehyde (MDA)[3].Quetiapine (10, 30, 100mg/kg; po; bid; 28d) elicited a statistically significant, dose-dependent decrease in METH-induced hyperlocomotion 0.5h after administration. There were Quetiapine-induced, dose-dependent decreases in locomotor activity at 8 and 12h[4].
References:
[1].Cross A J, Widzowski D, Maciag C, et al. Quetiapine and its metabolite norQuetiapine: translation from in vitro pharmacology to in vivo efficacy in rodent models[J]. British journal of pharmacology, 2016, 173(1): 155-166.
[2].Mi G, Wang Y, Ye E, et al. The antipsychotic drug Quetiapine stimulates oligodendrocyte differentiation by modulating the cell cycle[J]. Neurochemistry International, 2018, 118: 242-251.
[3]. Xu P, Zhang M, Wang X, et al. Antioxidative effect of Quetiapine on acute ultraviolet-B-induced skin and HaCaT cell damage[J]. International Journal of Molecular Sciences, 2018, 19(4): 953.
[4] Kondo M A, Tajinda K, Colantuoni C, et al. Unique pharmacological actions of atypical neuroleptic Quetiapine: possible role in cell cycle/fate control[J]. Translational psychiatry, 2013, 3(4): e243-e243.
Quetiapine是一种5-HT受体激动剂，对人类5-HT1A受体的pEC50为4.77。Quetiapine是一种多巴胺受体拮抗剂，对人类D2受体的 pIC50为6.33。Quetiapine是一种非典型抗精神病药，用于治疗精神分裂症、躁郁症和重度抑郁症[1]。
Quetiapine（1，10μM；48h）导致细胞周期退出并促进原代少突胶质细胞培养中的细胞分化[2]。Quetiapine（10，20，50μg/mL；12h）处理的MDA水平显著降低，SOD和GSH-Px活性显著升高[3]。Quetiapine（<100μM；24h）对细胞活力没有显著影响[4]。
Quetiapine（400mg/mL；surface application；0、6、12、24h）治疗能够显著减少UVB刺激引起的皮肤增厚、红斑和水肿以及炎症。此外，Quetiapine治疗可增加抗氧化酶的活性，包括超氧化物歧化酶 (SOD)和谷胱甘肽过氧化物酶(GSH-Px)，同时减少了氧化脂质丙二醛 (MDA) 的产生[3]。Quetiapine（10、30、100mg/kg；po；bid；28d）在给药后0.5小时引起METH诱导的过度运动出现统计学上显著的剂量依赖性下降。在8小时和12小时，Quetiapine诱导的运动活性出现剂量依赖性下降[4]。