Neuroprotective activity of Phoenixsylvestris against colchicine induced neuroinflammation and cognitive deficits in rat

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Parvati Suryvanshi, Chandrashekhar V M, Basavaraj Lalasangi, Mallappa Shalavadi, Lingaraj A, Ashok Gnanasekaran, Rajesh Thangarajan, Pugazhandhi Bakthavatchalam


Introduction: Colchicine induced neuro-inflammation and cognitive deficits can be cured by the Phoenix sylvestris.

Objectives: The present study was designed to evaluate the neuroprotective effect of Phoenix sylvestris against colchicine induced Neuroinflammation and cognitive deficits in rats.

Methods: Neuroprotective activity was carried out by colchicine induced Neuroinflammation and cognitive deficits on rats. Test group animals administrated with ethanol extract Phoenix sylvestris (EPS) at dose of 150 mg/kg, 300 mg/kg, and 500mg/kg for 28 days. Neurobehavioral tests like Morris water maze, Elevated plus maze, Radial arm maze were performed. Inflammatory mediators like TNF-∝, IL-6 were assessed. Followed by biochemical parameter such as LPO, GSH, SOD, CAT, total thiols and ACh were assessed and histopathology of brain tissue were studied on the final day of the experiment.

Results: EPS shows a dose dependent neuroprotective activity with significant decrease in time latency of Morris water maze, elevated plus maze and radial arm maze in EPS treated group compared to colchicine induced control group. Inflammatory mediators showed decrease in TNF-α, increase in IL-6. Biochemical estimations showed significant decreases in LPO and increased in SOD, CAT, GSH, total thiols & Ach level in the EPS treated group as compared with colchicine induced control group. Molecular docking results showed main constituents of Phoenix sylvestris could interact with TACE and AChE.

Conclusions: EPS treatment could reduce neuroinflammation and preventing the development of cognitive deficits. In conclusion, the present study suggests that administration of EPS possesses neuroprotective activity against colchicine induced Neuroinflammation and cognitive deficits.

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