L-Theanine Attenuates LPS Induced Motor deficit in Experimental Rat Model of Parkinson’s Disease: Emphasis on Mitochondrial activity, Neuroinflammation and Neurotransmitters

Abstract

\n Parkinson’s disease (PD) is a neurodegenerative disorder characterized by the loss of dopamine neurons in the substantia nigra. The pathogenesis of PD, including oxidative stress, mitochondrial dysfunction, neuroinflammation, and neurotransmitter dysregulation. L-theanine is an amino acid found in green tea and has antioxidant, anti-inflammatory, and neuroprotective effects with a high BBB permeability. Therefore, the current study was designed to investigate the possible neuroprotective effect of L-theanine in lipopolysaccharide (LPS) induced motor deficits and striatal neurotoxicity in a rat model of PD. LPS was infused at a dose of 5 µg/5 µl PBS, stereotaxically into SNpc of rats. Treatment with L-theanine at (50 and 100 mg/kg; po), and Sinemet (36 mg/kg; po) was given from day 7 to 21 in of LPS injected rat. On a weekly basis all behavioral parameters were assessed, and animals were sacrificed on day 22. The striatum tissue of brain was isolated for biochemicals (Nitrite, GSH, catalase, SOD, mitochondrial complexes I and IV), neuroinflammatory markers (IL-1β, TNF-α, and IL-6), and neurotransmitters (serotonin, dopamine, norepinephrine, GABA, and glutamate) estimations. Results revealed that L-theanine dose-dependently and significantly reversed motor deficits, assessed through locomotor and rotarod activity. Moreover, L-theanine attenuated biochemical markers, reduced oxidative stress, and neurotransmitters dysbalance in the brain. L-theanine treatment at 100 mg/kg; po substantially reduced these pathogenic events by increasing mitochondrial activity, restoring neurotransmitter levels, and inhibiting neuroinflammation. Moreover, data suggest that the positive effects of L-theanine on motor coordination may be mediated by the suppression of nuclear factor-κB (NF-κB) induced by LPS.