Title : Neuroprotective potential of a traditional Uttarakhand plant against lambda-cyhalothrin-induced neural impairment: A pharmacological investigation
Abstract:
Neurodegenerative disorders are a group of diseases characterized by the progressive loss of structure or function of neurons, including brain cells, leading to impaired movement, cognition, and other neurological functions. Several factors contribute to the progression of neurodegeneration. Compelling evidence indicates that pesticide exposure is associated with an increased risk of neurodegenerative diseases, as many pesticides are identified as neurotoxic. Neurodegeneration was induced by Pyrethroid insecticides, particularly Lambda-Cyhalothrin (LCT) which are extensively used due to their high potency as insecticides and relatively low mammalian toxicity at recommended doses. However, accumulating evidence suggests that LCT exposure induces neurotoxicity through mechanisms involving oxidative stress, mitochondrial dysfunction, neuroinflammation, and neuronal apoptosis. Crude extract of Pyracantha Crenulata was prepared to mitigate the effect of pesticide using cold maceration method. To evaluate the neuroprotective efficacy of PCEA through a combination of behavioural, biochemical, molecular, and histopathological analyses. Behavioural assessments, including locomotor activity, cognitive performance (Morris water maze), and recognition assessment, were conducted to determine functional recovery following PCEA treatment. Biochemical estimations focused on key markers of oxidative stress (Malondialdehyde (MDA), reduced Glutathione (GSH)), cholinergic function (acetylcholinesterase activity), and nitrosative stress (nitric oxide levels). Furthermore, the modulatory effects of PCEA on Neuroinflammatory Cytokines (TNF-α, IL-6) and Neurotrophic Factors (BDNF) were assessed to elucidate its anti-inflammatory and neurorestorative properties. This study represents the first comprehensive investigation into the neuroprotective potential of P. crenulata against LCT-induced neurotoxicity, using acute (6 days; 4 mg/kg, 8 mg/kg) and chronic (28 days; 2 mg/kg) exposure models. Our findings not only establish dose-dependent neurotoxicity thresholds for LCT but also highlight P. crenulata’s ability to mitigate oxidative damage, suppress neuroinflammation, and preserve neuronal architecture.
