Inhibition of phosphodiesterase 4 by FCPR16 protects SH-SY5Y cells against MPP⁺-induced decline of mitochondrial membrane potential and oxidative stress.

ABSTRACT: Phosphodiesterase 4 (PDE4) is a promising target for the treatment of Parkinson's disease (PD). However, the underlying mechanism has not yet been well elucidated. Additionally, most of current PDE4 inhibitors produce severe nausea and vomiting response in patients, which limit their clinical application. FCPR16 is a novel PDE4 inhibitor with little emetic potential. In the present study, the neuroprotective effect and underlying mechanism of FCPR16 against cellular apoptosis induced by 1-methyl-4-phenylpyridinium (MPP⁺) were examined in SH-SY5Y cells. FCPR16 (12.5-50 μM) dose-dependently reduced MPP⁺-induced loss of cell viability, accompanied by reductions in nuclear condensation and lactate dehydrogenase release. The level of cleaved caspase 3 and the ratio of Bax/

SUBMITTER: Zhong J 

PROVIDER: S-EPMC5842311 | biostudies-literature | 2018 Jun

REPOSITORIES: biostudies-literature