Neuroscience letters · 2025
Impact of Corn Silk Extract on paclitaxel-induced spinal cord and sciatic nerve injuries in rats: Biochemical and histological evaluation.
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Badr Nada S, El-Nabi Sobhy Hassab, El-Gerbed Mohamed S A
Аннотация
BACKGROUND: Overactivation of the Renin-Angiotensin System (RAS) is linked to oxidative stress and inflammation, contributing to the pathogenesis of Paclitaxel-Induced Peripheral Neuropathy (PIPN). Corn Silk Extract (CSE) exhibits neuroprotective activity through its antioxidant, anti-inflammatory, and anti-apoptotic properties. This study aims to evaluate the protective effects of CSE against PIPN through the modulation of oxidative, inflammatory, and RAS-related signals.
MATERIAL AND METHODS: CSE was analyzed for its phenolic and flavonoid content and its antioxidant activity. The study involved four experimental groups: Control, CSE (400 mg/kg/day), Paclitaxel (PTX) (2 mg/kg, i.p. on days 1st, 3rd, 5th, and 7th), and PTX + CSE. Behavioral tests, biochemical analyses, histological evaluations, and molecular docking were conducted to assess the effects of CSE.
RESULTS: PTX-induced hyperalgesia, increased nitric oxide, nuclear factor kappa B (NF-κB), Myeloperoxidase (MPO), Angiotensin-Converting Enzyme (ACE), angiotensin II, aldosterone, high mobility group box 1 protein, and decreased glutathione, total antioxidant capacity, and inhibitor of nuclear factor kappa B alpha. It induced spinal cord and sciatic nerve neuron damage, axonal demyelination, and reduced Schwann cells number. CSE administration with PTX improved behavioral responses, reduced oxidative and inflammatory markers, restored antioxidant and RAS signal balance, and preserved nerve tissue structure. Docking showed strong binding of CSE components with NF-κB, MPO, and ACE, suggesting direct inhibitory interactions.
CONCLUSION: CSE attenuates PINP by reducing oxidative stress, inflammation, and RAS dysregulation while preserving neuronal and nerve structure. In silico results support the effects of CSE components on multiple inflammatory pathways, highlighting its therapeutic potential.
MATERIAL AND METHODS: CSE was analyzed for its phenolic and flavonoid content and its antioxidant activity. The study involved four experimental groups: Control, CSE (400 mg/kg/day), Paclitaxel (PTX) (2 mg/kg, i.p. on days 1st, 3rd, 5th, and 7th), and PTX + CSE. Behavioral tests, biochemical analyses, histological evaluations, and molecular docking were conducted to assess the effects of CSE.
RESULTS: PTX-induced hyperalgesia, increased nitric oxide, nuclear factor kappa B (NF-κB), Myeloperoxidase (MPO), Angiotensin-Converting Enzyme (ACE), angiotensin II, aldosterone, high mobility group box 1 protein, and decreased glutathione, total antioxidant capacity, and inhibitor of nuclear factor kappa B alpha. It induced spinal cord and sciatic nerve neuron damage, axonal demyelination, and reduced Schwann cells number. CSE administration with PTX improved behavioral responses, reduced oxidative and inflammatory markers, restored antioxidant and RAS signal balance, and preserved nerve tissue structure. Docking showed strong binding of CSE components with NF-κB, MPO, and ACE, suggesting direct inhibitory interactions.
CONCLUSION: CSE attenuates PINP by reducing oxidative stress, inflammation, and RAS dysregulation while preserving neuronal and nerve structure. In silico results support the effects of CSE components on multiple inflammatory pathways, highlighting its therapeutic potential.