Abstract
PurposeIntranasal administration of phospholipid-based gelatin nanoparticles (GNP) was prepared to investigate the neuro-recovery effects of neuropeptide Substance P (SP) on hemiparkinsonian rats.MethodsThe SP-loaded gelatin nanoparticles (SP-GNP) were prepared by a water-in-water emulsion method and possessed high stability, encapsulating efficiency and loading capacity. PC-12 cells were used to examine the growth enhancement of SP-GNP in vitro by MTT assays and flow cytometry (FCM). The therapeutic effects of SP-GNP on 6-hydroxydopamine (6-OHDA) induced hemiparkinsonian rats were assessed by quantifying rotational behavior and the levels of tyrosine hydroxylase (TH), phosphorylated c-Jun protein (p-c-Jun) and Caspase-3 (Cas-3) expressed in substantia nigra (SN) region of hemiparkinsonian rats.ResultsPC-12 cells under SP-GNP treatment showed better cell viability and lower degree of apoptosis than those under SP solution treatment. Hemiparkinsonian rats under intranasal SP-GNP administration demonstrated better behavioral improvement, higher level of TH in SN along with much lower extent of p-c-Jun and Cas-3 than those under intranasal SP solution administration and intravenous SP-GNP administration.ConclusionsWith the advantages of GNP and nose-to-brain pathway, SP can be effectively delivered into the damaged SN region and exhibit its neuro-recovery function through the inhibition on JNK pathway and dopaminergic neuron apoptosis.
Highlights
Parkinson’s disease (PD) is a chronic disorder of the central nervous system (CNS)
The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript
With the advantages of gelatin nanoparticles (GNP) and nose-to-brain pathway, Substance P (SP) can be effectively delivered into the damaged substantia nigra (SN) region and exhibit its neuro-recovery function through the inhibition on Jun N-terminalkinase (JNK) pathway and dopaminergic neuron apoptosis
Summary
Parkinson’s disease (PD) is a chronic disorder of the central nervous system (CNS). PD is caused primarily by progressive loss of dopaminergic cells in the substantia nigra (SN) region, which leads to bradykinesia, muscular rigidity, resting tremor, and postural instability[1, 2]. SP-containing neurons are widely distributed throughout the central and peripheral nervous systems, especially in the SN region [5]. After SP or SP receptor antagonist treatment for the rat model of Parkinson's disease, the content of striatal dopamine and its metabolites increase, and PD symptoms improve [9, 10]. In rats with substantia nigra partially damaged by 6-0HDA, systemic administration of SP before and after the damage promotes functional recovery of Parkinson's disease [10, 11]
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