Background:

Benserazide hydrochloride (Serazide) is commonly used in Parkinson's disease and is an inhibitor of peripheral aromatic L-amino acid decarboxylase (AADC)[1].

Benserazide hydrochloride (BH) and Levodopa (LD) individually and in combination (Benserazide hydrochloride?+?LD) (25 μM; 0 hour, 12 hours, 24 hours and 168 hours; SH-SY5Y) treatment inhibit protein aggregation and have the ability to minimise the amyloid-induced cytotoxicity in human neuroblastoma cell line. Benserazide hydrochloride and LD both can act as efficient inhibitors of the formation of cytotoxic HSA aggregates, and the inhibitory effects are more pronounced when both of these drugs are added simultaneously[2].

Benserazide (5-50 mg/kg; intraperitoneal injection; male Wistar rats) treatment of 6-OHDA-lesioned rats increases exogenous L-DOPA-derived extracellular DA levels, the time to reach the peak DA levels are significantly prolong by Benserazide dose-dependently. The AADC activity in the denervates striatal tissues shows a significant decrease by 10 mg/kg and 50 mg/kg Benserazide. Benserazide reduces the central AADC activity in the striatum of rats with nigrostriatal denervation, which leads to changes in the metabolism of exogenous L-DOPA[1].

参考文献:
[1]. Shen H, et al. Effects of benserazide on L-DOPA-derived extracellular dopamine levels and aromatic L-amino acid decarboxylase activity in the striatum of 6-hydroxydopamine-lesioned rats. Tohoku J Exp Med. 2003 Mar;199(3):149-59.
[2]. Chandel TI, et al. A multiparametric analysis of the synergistic impact of anti-Parkinson's drugs on the fibrillation of human serum albumin. Biochim Biophys Acta Proteins Proteom. 2019 Mar;1867(3):275-285.