Taurine, an essential amino acid, attenuates rotenone-induced Parkinson's disease in rats by inhibiting alpha-synuclein aggregation and augmenting dopamine release.

Abstract

Reducing antioxidant levels exacerbates the generation of reactive oxygen/nitrogen species, leading to alpha-synuclein aggregation and the degeneration of dopaminergic neurons. These play a key role in the onset of Parkinson's disease (PD), for which effective treatment remains elusive. This study examined the neuroprotective effects of taurine, an essential β-amino acid with antioxidant and antiinflammation properties, in Swiss male mice exposed to rotenone-induced PD. Mice (20-25 g) were grouped into seven groups (n = 9) and treated with taurine alone (5, 10 and 20 mg/kg, p.o) or levodopa (10 mg/kg, p.o) for 28 consecutive days following intraperitoneal co-administration of rotenone (1.5 mg/kg, in 5 % dimethylsulfoxide) for 14 alternate days. Open-field, rota-rod and hanging-wire motor performance and coordination tests were conducted on days 26-28. Oxidative stress and neuroinflammatory markers; levels of acetylcholinesterase enzyme activity, dopamine, and alpha-synuclein were assayed in the striatal and prefrontal-cortical regions alongside histological examinations. Rotenone significantly reduced latency to fall and akinesia-like behavior with several slip/error relative to vehicle groups. Taurine increased the latency to fall, notably improving motor coordination, locomotor deficit, and neuromuscular competence. Also, rotenone significantly increased malondialdehyde and nitrite; while decreasing acetylcholinesterase activity, glutathione, catalase, superoxide-dismutase, and glutathione-S-transferase levels in the striatum and prefrontal-cortex respectively, which were attenuated by taurine. Taurine increased dopamine levels in the striatum and prefrontal cortex dose-independently. Like carbidopa, taurine decreased alpha-synuclein, tumor-necrosis factor-α and interleukin-6 levels in the striatum and prefrontal-cortex. Additionally, taurine-reversed rotenone-induced neurodegeneration in the striatum and prefrontal cortex indicates neuroprotective function. Conclusively, taurine attenuates rotenone-induced PD-like behavior by enhancing the brain's antioxidant system, inhibiting pro-inflammatory cytokine release, reducing α-synuclein formation, and augmenting dopaminergic release in mice's brains.