Protective effect of hydroxysafflor yellow A on dopaminergic neurons against 6-hydroxydopamine, activating anti-apoptotic and anti-neuroinflammatory pathways.

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ContextHydroxysafflor yellow A (HSYA) has been shown to have neuroprotective effects in cerebral infarction. However, its underlying roles in apoptosis and inflammation in Parkinson's disease (PD) are unknown.ObjectiveThe present study investigates the effects and underlying mechanisms of HSYA on dopaminergic (DA) neurodegeneration, inflammation, and apoptosis.Materials and methodsThe PD model was established by 2 μL of 6-hyroxydopamine (6-OHDA) (3 μg/μL) striatal injection in C57BL/6J mice with different doses of HSYA (2, 4, or 8 mg/kg). In vitro, after being treated with HSYA for 1 h, SH-SY5Y cells were exposed to 6-OHDA for 24 h before analysis. Expression of tyrosine hydroxylase (TH) in substantia nigra (SN) and corpus striatum (STR) was evaluated by immunohistochemistry (IHC) and western blot. In addition, apoptosis-related and inflammatory proteins were examined by western blot.ResultsAdministration of HSYA significantly reduced the Apomorphine (APO)-induced rotation, decreased from 122.5 ± 15.1 (6-OHDA group) to 47.2 ± 14.3 (8 mg/kg HSYA group). HSYA partially restored a deficit in the SN and STR of PD mice brains in TH. Furthermore, western blot analysis revealed that HSYA reduced inflammatory proteins, including iNOS, COX-2 and NF-κB and attenuated the elevation of DA neuronal apoptosis observed in PD. In vitro assays showed that HSYA reduced the levels of p-p38 and p-JNK and increased that of p-ERK in 6-OHDA-leisoned SH-SY5Y cells.ConclusionsThese findings indicate that HSYA protects against 6-OHDA induced DA neurodegeneration partly by regulating the MAPK inflammatory signalling pathway and apoptosis which highlight its therapeutic potential in the treatment of PD.

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