Gastrodin microinjection suppresses 6-OHDA-induced motor impairments in parkinsonian rats: insights into oxidative balance and microglial activation in SNc
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Purpose of the research
In this study, we appraised the effect of pre-treatment with intra-cerebro ventricular (i.c.v) microinjection of gastrodin (Gst) on catalepsy, motor imbalance, substantia nigra pars compacta (SNc) myeloperoxidase (MPO) activity, lipid peroxidation levels, nitric oxide (NO) production and total antioxidant capacity (TAC) in 6-hydroxydopamine (6-OHDA) rats model of PD.
Materials and methods
Male Wistar rats were pre-treated with i.c.v microinjections of Gst (20, 40 and 80 μg/3 μl/rat) for five consecutive days. Then, catalepsy and motor balance were induced by unilateral infusion of 6-OHDA (8 μg/2 μl/rat) into the SNc. The anti-cataleptic and motor balance improving effect of Gst was assessed by the Bar test and Rotarod 3 weeks after neurotoxin injection, respectively. SNc MPO activity and lipid peroxidation levels, NO production and TAC were assessed at the end of behavioral experiments.
Our data demonstrated that Gst pre-treatment significantly (p < 0.001) was prevented motor in-coordination and catalepsy in neurotoxin lesioned rats. The most motor improving effect was seen at 80 μg Gst (p < 0.001). Pre-treatment of parkinsonian rats with Gst meaningfully (p < 0.001) was suppressed MPO activity, lipid peroxidation and NO production. Furthermore, the TAC level in the SNc was increased (p < 0.001) in Gst-microinjected rats about to the normal non-parkinsonian animals.
In summary, pre-treatment with Gst abolished 6-OHDA-induced catalepsy and improved motor incoordination by decreasing: SNc MPO activity, lipid peroxidation levels and NO production, and restoring SNc levels of TAC to the levels of healthy rats.
KeywordsGastrodin Catalepsy Rotarod Myeloperoxidase MDA Parkinson disease Rat
Compliance with ethical standards
Conflict of interest
The authors declare that they have no competing interest.
- Cohen G (1994) Free radicals, oxidative stress and neurodegeneration. In: Calne DB (ed) Neurodegenerative diseases. W. B Saunders, Philadelphia, pp 139–161Google Scholar
- Dexter DT, Jenner P (2013) Parkinson disease: from pathology to molecular disease mechanisms. Free Radic Biol Med 62:132–144. https://doi.org/10.1016/j.freeradbiomed.2013.01.018 CrossRefPubMedGoogle Scholar
- Haddadi R, Nayebi AM, Farajniya S, Brooshghalan SE, Sharifi H (2014) Silymarin improved 6-OHDA-induced motor impairment in hemi-parkisonian rats: behavioral and molecular study DARU. J Pharm Sci 22:38Google Scholar
- Ikawa M et al (2017) Dopaminergic neuronal oxidative stress is increased with disease progression in patients with Parkinson’s disease: a study with PET and SPECT: P4. 027Google Scholar
- Paxinos G, Watson C (2007) The rat brain in stereotaxic coordinates. Academic press, San DiegoGoogle Scholar