LAUSR

Parkinson's disease (PD) is a neurodegenerative disease which results in damage in neuronal cells. Insulin‐like growth factor (IGF)‐1 was previously reported to play a role of neuroprotection in some diseases. Nitric oxide (NO) can also regulate neuronal cells. However, the mechanisms underlying IGF‐1 and NO in PD still need to be elucidated. In present study, we explored the interaction between IGF‐1 and inducible Nitric‐Oxide Synthase (iNOS) in PD progression. We firstly constructed PD models by methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP) or MPP+ treatment. Then RT‐qPCR revealed that IGF‐1 expression was downregulated while iNOS expression was upregulated in MPTP model. Moreover, IGF‐1 elevation or iNOS depletion enhanced cell viability and blocked cell apoptosis. Rescue assay disclosed iNOS overexpression reversed the effect on viability and apoptosis mediated by IGF‐1 upregulation. Furthermore, IGF‐1 was identified to positively regulate miR‐302b‐5p which could target iNOS. MiR‐302b‐5p could abolish the inhibitory function IGF‐1 exerted on cell apoptosis and iNOS could counteract miR‐302b‐5p upregulation‐triggered inhibition on cell apoptosis as well. Besides, we observed the deficiency of miR‐302b‐5p improved the lesioned neurobehavior of MPTP‐treated mice. To sum up, present study proved that miR‐302b‐5p enhanced the neuroprotective effect of IGF‐1 in MPTP‐induced PD by regulating iNOS, recommending a novel therapeutic target for PD treatment.