Loganin Attenuates Rotenone-Induced Parkinsonism-like Features in Rats Through Multi-Target Neuroprotective...

Area of Science:

• Neuroscience
• Pharmacology
• Biochemistry

Background:

• Rotenone (RT) neurotoxicity models Parkinsonism, inducing oxidative stress, mitochondrial dysfunction, neuroinflammation, and dopaminergic deficits.
• Loganin (LG), from Cornus officinalis, exhibits known antioxidant, anti-inflammatory, and neuroprotective properties.
• LG's protective effects in RT-induced Parkinsonism models require further elucidation.

Purpose of the Study:

• To investigate the neuroprotective potential of Loganin (LG) against rotenone (RT)-induced Parkinsonism-like pathology in rats.
• To explore the involvement of antioxidant-related signaling mechanisms in LG's protective effects.

Main Methods:

• Adult male Wistar rats received stereotaxic rotenone (RT) injection to induce unilateral nigrostriatal injury.
• Loganin (LG) was administered orally daily for 21 days at varying doses (3, 10, 30 mg/kg).
• Behavioral and biochemical analyses assessed motor function, oxidative stress, mitochondrial function, inflammation, apoptosis, and catecholamine levels.

Main Results:

• RT induced significant motor deficits, oxidative stress, mitochondrial dysfunction, neuroinflammation, apoptosis, and altered striatal catecholamines.
• LG treatment dose-dependently attenuated RT-induced pathological changes, with optimal effects at 10 and 30 mg/kg.
• Co-administration with trigonelline (TG) partially reduced LG's benefits, suggesting antioxidant signaling involvement.

Conclusions:

• Loganin (LG) exhibits multi-target neuroprotective effects against rotenone-induced Parkinsonism-like features in rats.
• LG's protective actions are linked to the attenuation of oxidative stress, mitochondrial dysfunction, neuroinflammation, apoptosis, and catecholaminergic disturbances.
• Further molecular validation is required to establish LG as a disease-modifying candidate for Parkinson's disease.