Calpastatin reduces methamphetamine-induced induction in c-Jun phosphorylation, Bax and cell death in neuroblastoma SH-SY5Y cells

Methamphetamine (METH) is one of the most commonly abused substances in today's society. Many studies have shown that the process of cell death induced by METH involves with the reception of death signals, an increase in pro-apoptotic proteins (Bax) and an activation of cysteine protease death pathway. The objective of this study was to investigate the neuroprotective effects of calpastatin against METH-induced toxicity in SH-SY5Y neuroblastoma cells by observing cell viability, phosphorylation of transcription factor, c-Jun (phospho-c-Jun) and levels of Bax and Bcl-2. The results showed that METH significantly decreased cell viability in SH-SY5Y cultured cells. Conversely, increase in phospho-c-Jun and Bax/Bcl-2 ratio was observed in METH-treated cells. Calpastatin reversed the toxic effect of METH by increasing cell viability, reducing phospho-c-Jun and Bax/Bcl-2 ratio in METH-treated cells. These results indicated that calpastatin has the capacity to reverse an activation of the death process in METH-treated dopaminergic cell lines.

► Methamphetamine can cause a reduction in cell viability in SH-SY5Y cell cultures. ► Methamphetamine can induce induction in c-Jun-phosphorylation and Bax/Bcl-2 ratio in SH-SY5Y cell cultures. ► Calpastatin can abolish the toxic effects of methamphetamine in SH-SY5Y cultured cells.