4.7 Article

Boswellia serrata suppress fipronil-induced neuronal necrosis and neurobehavioral alterations via promoted inhibition of oxidative/inflammatory/apoptotic pathways

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SCIENCE OF THE TOTAL ENVIRONMENT
卷 785, 期 -, 页码 -

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ELSEVIER
DOI: 10.1016/j.scitotenv.2021.147384

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Boswellia serrata; Fipronil; Glial fibrillary acidic protein; Lipid peroxidation; Brain; Neuronal death

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Boswellic acid (BA) is a powerful compound known for its antioxidant, anti-inflammatory, and anticancer properties, derived from the gum-resin of Boswellia serrate. The study demonstrates that Boswellia serrata extract can protect against neurobehavioral toxicity induced by fipronil in male albino rats, showing significant neuroprotective effects by modulating oxidative, inflammatory, and apoptotic pathways.
Boswellic acid (BA) is a pentacyclic terpenoid derived from the gum-resin of Boswellia serrate. It is known for its strong antioxidant, anti-inflammatory, and anticancer properties. It has improved spatial learning and provides neuroprotection against trimethyltin-induced memory impairment. The aim of this study is to evaluate the possible neuroprotective activity of B. serrata extract (BSE) containing BA against fipronil (FPN)-induced neurobehavioral toxicity in Wister male albino rats. Sixty male rats were allocated equally into six groups. The first group served as control; the second and third groups received BSE at two different oral doses (250 or 500 mg/kg body weight [BW], respectively). The fourth group was orally intoxicated with FPN (20 mg/kg BW), whereas the fifth and sixth groups served as preventive groups and co-treated with FPN (20 mg/kg BW) and BSE (250 or 500 mg/kg BW, respectively). The experiment was conducted over 8 weeks period. Results revealed that co-treatment with BSE led to significant (p > 0.05) dose-dependent reduction in malondialdehyde (MDA), nitric oxide (NO), interleukin-6 (IL6), tumor necrosis factors-alpha (TNF-alpha), nuclear factor Kappa-B (NF-KB), Cyclooxegenase-2 (COX-2), prostaglandin E2 (PGE2), serotonin, and acetylcholine (ACh). Conversely, significant (p > 0.05) up regulation of catalase (CAT), glutathione peroxidase (GSH-Px), gamma-aminobutyric acid (GABA), and acetylcholine esterase (AChE) has reported in BSE-co-treated groups. In addition, significant (p > 0.05) promotion in neurobehaviours, histopathologic imaging of the cerebral, cerebellar, and hippocampal regions, and immunohistochemical expression of caspase-3 and glial fibrillary acidic protein (GFAP) were also reported in the BSE-treated groups in a dose-dependent manner. In conclusion, BSE (500 mg/kg BW) is a natural, promising neuroprotective agent that can mitigate FPN-induced neurobehavioral toxicity via the suppression of oxidative, inflammatory, and apoptotic pathways and relieve neuronal necrosis and astrogliosis. (c) 2021 Elsevier B.V. All rights reserved.

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