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Background    L-dopa (Levodopa) is well known for managing PD (Parkinson’s disease); however, its prolonged use caused dyskinesia (LID). Due to the varied presentation of LID, effective treatment options are scarce. Flavonoids reported their neuroprotective activity by ameliorating acetylcholinesterase, monoamine oxidase, and neuroinflammation. Kaempferol is another flavonoid bearing these potentials.Aim    To evaluate neuroprotective activity of kaempferol in dyskinetic rats.Methods    PD was developed in Sprague-Dawley rats by injecting combination of L-ascorbic acid (10 µL) + 6-OHDA (12 µg) in medial forebrain bundle to induce neuronal damage in substantial nigra (SNr). LID was induced by administrating combination of L-dopa (20 mg/kg) + benserazide HCl (5 mg/kg) for 42 days. Rats were concomitantly treated with amantadine (40 mg/kg) or kaempferol (25, 50, and 100 mg/kg, p.o.).Results    Kaempferol (50 and 100 mg/kg) markedly ( p  &lt; 0.05) inhibited LID-induced abnormal involuntary movements (AIMs) and alternation in motor function. Kaempferol administration considerably ( p  &lt; 0.05) inhibited reduced mitochondrial complex activities, serotonin and dopamine levels, Bcl-2, and Tyrosine hydroxylase protein expressions in SNr. Additionally, kaempferol considerably ( p  &lt; 0.05) attenuated increased cFOS, FosB, Parkin, and Pdyn mRNAs expressions, Bax, cleaved caspase-3, caspase-3, and pJNK proteins levels; DOPAC and 5-HIAA levels in SNr. A positive correlation was reported between cFOS, FosB, Parkin, Pdyn, apoptosis, and TH with AIMs.Conclusion    Kaempferol effectively attenuated L-dopa-induced AIMs and dyskinesia via amelioration of alterations in cFOS, FosB, Parkin, Pdyn, Tyrosine hydroxylase, and apoptosis in the brain SNr.

Kaempferol ameliorated levodopa-induced dyskinesia in experimental rats: A role of brain monoamines, cFOS, FosB, Parkin, Pdyn, TH, and p-JNK