Please use this identifier to cite or link to this item: http://hdl.handle.net/10397/61183
Title: Protection against MPP+-induced neurotoxicity in SH-SY5Y cells by tormentic acid via the activation of PI3-K/Akt/GSK3β pathway
Authors: Zhao, Q
Ye, J
Wei, N
Fong, C
Dong, X
Keywords: MPP+
Neuroprotection
Parkinson's disease
PI3-K/Akt/GSK3
SH-SY5Y cells
Tormentic acid
Issue Date: 2016
Publisher: Pergamon Press
Source: Neurochemistry international, 2016, v. 97, p. 117-123 How to cite?
Journal: Neurochemistry international 
Abstract: The cause of Parkinson's disease (PD) could be ascribed to the progressive and selective loss of dopaminergic neurons in the substantia nigra pars compacta, and thus molecules with neuroprotective ability may have therapeutic value against PD. In the current study, the neuroprotective effects and underlying mechanisms of tormentic acid (TA), a naturally occurring triterpene extracted from medicinal plants such as Rosa rugosa and Potentilla chinensis, were evaluated in a widely used cellular PD model in which neurotoxicity was induced by MPP+ in cultured SH-SY5Y cells. We found that TA at 1-30 μM substantially protected against MPP+-induced neurotoxicity, as evidenced by the increase in cell viability, decrease in lactate dehydrogenase release and the reduction in apoptotic nuclei. Moreover, TA effectively inhibited the elevated intracellular accumulation of reactive oxygen species as well as Bax/Bcl-2 ratio caused by MPP+. Most importantly, TA markedly reversed the inhibition of protein expression of phosphorylated Akt (Ser 473) and phosphorylated GSK3β (Ser 9) caused by MPP+. LY294002, the specific inhibitor of PI3-K, significantly abrogated the up-regulated phosphorylated Akt and phosphorylated GSK3β offered by TA, suggesting that the neuroprotection of TA was mainly dependent on the activation of PI3-K/Akt/GSK3β signaling pathway. The results taken together indicate that TA may be a potential candidate for further preclinical study aimed at the prevention and treatment of PD.
URI: http://hdl.handle.net/10397/61183
ISSN: 0197-0186
DOI: 10.1016/j.neuint.2016.03.010
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