Phytochemical Standardization and Neuroprotective Potential of Celastrus paniculatus Seed Extract Against Amyloid-β-Induced Neuronal Injury: Insights into Oxidative and Cholinergic Dysfunction

Phytochemical Standardization and Neuroprotective Potential of Celastrus paniculatus Seed Extract Against Amyloid-β-Induced Neuronal Injury: Insights into Oxidative and Cholinergic Dysfunction

Authors

  • ¹Rajapandi Raju, ²Basu Venkateswara Reddy, ³Neelmani Chauhan*, ⁴Mohan Verma, ⁵Zufnoon Khan, ⁶Amrita Thakur, ⁷Avinash S Jiddewar, ⁸Erigi Nikhil Chakravarthy

Keywords:

Celastrus paniculatus; amyloid-β1–42; neuroprotection; acetylcholinesterase; oxidative stress; SH-SY5Y cells; phytochemical standardization

Abstract

Celastrus paniculatus has traditionally been associated with cognitive and neurological benefits; however, integration of phytochemical standardization with mechanistic evaluation of its neuroprotective activity remains important. This study investigated the phytochemical characteristics, antioxidant activity, acetylcholinesterase (AChE) inhibition, and neuroprotective potential of a hydroalcoholic extract of C. paniculatus seeds (CPHE) against amyloid-β1–42 (Aβ1–42)-induced injury in differentiated SH-SY5Y cells. CPHE showed an extraction yield of 12.74% and contained 68.42 ± 2.31 mg GAE/g total phenolics and 31.76 ± 1.48 mg QE/g total flavonoids. HPLC-PDA analysis provided a characteristic multicomponent fingerprint. CPHE exhibited concentration-dependent DPPH and ABTS radical-scavenging activities, with IC50 values of 61.8 and 50.7 µg/mL, respectively, and inhibited AChE with an IC50 of approximately 70 µg/mL. Aβ1–42 exposure reduced neuronal cell viability to 65.6 ± 2.8%, whereas CPHE increased viability dose-dependently to 90.4 ± 2.3% at 100 µg/mL. CPHE also attenuated intracellular reactive oxygen species and cellular AChE activity while restoring superoxide dismutase, catalase, and reduced glutathione levels. These findings demonstrate that standardized CPHE provides significant in vitro neuroprotection against Aβ1–42-induced neuronal injury, associated with complementary antioxidant and cholinesterase-modulating activities.

Downloads

Published

2026-09-24

Issue

Section

Articles

Citation Check

Loading...