Research articleInsulin on activation of autophagy with integrins and syndecans against MPP+-induced α-synuclein neurotoxicity

- Insulin inhibited MPP+-induced cell membrane damages.
- Insulin also inhibited the Cox-2 and α-synuclein levels.
- MPP+ and/or insulin enhanced the autophagy LC3.
- Insulin enhanced the ILK and induced the integrins β3, αV, syndecan-1 and -3.
- Insulin prevents MPP+-induced apoptosis in SH-SY5Y + RA cells.

Parkinson's disease (PD) is the second most common neurodegenerative disease in the elderly caused by dopaminergic neuronal cell death. Human neuroblastoma SH-SY5Y cells differentiated by retinoic acid have been used to study the in vitro PD model induced by 1-methyl-4-phenyl pyridinium (MPP+). In this study, pretreatment of insulin inhibited MPP+-induced cell membrane damages, which also inhibited the Cox-2 and α-synuclein levels. In addition, MPP+ and/or insulin enhanced the autophagy LC3. Furthermore, MPP+-induced neurotoxicity diminished the integrins β3, αV and induced the syndecan-1 and -3. Insulin pretreatment enhanced the phosphorylation of integrin-linked kinase and further induced the integrin and syndecan molecules. These findings suggest that insulin prevents MPP+-induced α-synuclein apoptosis through the activation of integrin and syndecan pathways in SH-SY5Y + RA cells.