Neuroprotective effect of Urukku Velichenna (Traditionally processed virgin coconut oil) in Parkinson's disease: Bridging ethnopharmacology and experimental validation using in vitro, in vivo, and in silico models.
Neuroprotective effect of Urukku Velichenna (Traditionally processed virgin coconut oil) in Parkinson's disease: Bridging ethnopharmacology and experimental validation using in vitro, in vivo, and in silico models.
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Original abstract
ETHNOPHARMACOLOGICAL RELEVANCE: Hot-Processed Virgin Coconut Oil (HPVCO) is a traditionally prepared form of Virgin Coconut Oil (VCO) obtained through a unique extraction method. This extraction is specific to certain villages in the state of Kerala, India.Traditionally, HPVCO has been used to treat various neurodegenerative diseases, however, experimental and mechanistic evidence for its role in Parkinson's disease (PD) is limited. AIM OF THE STUDY: The objective of the current research work is to assess the anti-Parkinson's activity of HPVCO in rotenone-induced SH-SY5Y cells, rat model of PD, and in silico models to investigate the underlying molecular mechanisms. MATERIALS AND METHODS: The components of HPVCO have been investigated by Gas chromatography-mass spectroscopy (GC-MS) analysis. Neuroprotective activity was investigated in SH-SY5Y cell lines and rat models using the neurotoxin rotenone. In the in vitro study, HPVCO (50 μg/mL) was administered to SH-SY5Y cells stimulated by rotenone (10 μM). Neuroprotection was assessed using dopamine levels, antioxidant markers (ROS and SOD), and anti-inflammatory markers (IL-6, IL-1β, TNF-α, and nitrite). In vivo, male Wistar rats (200-250 g, 10-12 weeks old) were treated with rotenone (2.5 mg/kg, intraperitoneally) for 10 days to induce PD, followed by daily oral administration of HPVCO (1306.4 mg/kg) for 21 days. On days 0, 7, 14, and 21, behavioral assays were performed, followed by histopathological evaluation. Antioxidant markers (ROS, SOD), anti-inflammatory markers (IL-6, IL-1β, TNF-α, nitrite), and dopamine levels were used to evaluate the neuroprotective effects. ADME analysis and network pharmacology were applied to identify potential therapeutic pathways related to lipid metabolism, oxidative stress, and neuroregulation. RESULTS: GC-MS analysis revealed 26 pharmacologically active phytoconstituents with antioxidant, anti-inflammatory, and neuroprotective activities. In in vitro, HPVCO displayed significant neuroprotective activity by reducing oxidative stress (ROS and SOD), neuroinflammation (IL-6, IL-1β, TNF-α, and nitrite), and increasing dopamine levels. Biochemical, histopathological, and behavioral assays in in vivo, supported the in vitro study results. Network and ADME analysis aligns with the dysregulated pathways central to PD, such as oxidative stress, neuroinflammation, and MAPK signaling. CONCLUSION: Antioxidant, anti-inflammatory, and neuroprotective bioactive compounds of HPVCO were identified through GC-MS analysis. Therefore, they might be accountable for the therapeutic benefits of HPVCO on PD.