Journal
JOURNAL OF CHEMICAL NEUROANATOMY
Volume 115, Issue -, Pages -Publisher
ELSEVIER
DOI: 10.1016/j.jchemneu.2021.101964
Keywords
Acrylamide; Silymarin; Oxidative stress; Monoamine neurotransmitters; Cathepsin
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Funding
- Deanship of Scientific Research at King Faisal University, Saudi Arabia [1811005]
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The study demonstrated that silymarin has a protective effect against acrylamide-induced cerebellar neurotoxicity in rats, alleviating oxidative stress and apoptosis. This provides new evidence for the potential applications of silymarin in preventing neurologic damage.
Background: Acrylamide (ACR) is a well-proven neurotoxin and potential food carcinogen in humans and rodent models. Silymarin (SIL) is a flavonoid mixture isolated from seeds, leaves, and fruits of Silymarin marianum (milk thistle) that possesses a free-radical scavenging effect.& nbsp; Objective: In this work, the primary focus was to investigate the efficacy of SIL to mitigate ACR-induced subacute neurotoxic effects and oxidative changes in rat cerebellum.& nbsp; Methods: Adult male rats were treated intraperitoneally with ACR (50 mg/kg) with or without SIL (160 mg/kg). The neuropathology and biochemical parameters viz. lipid peroxidation (measured as levels of malondialdehyde or MDA), catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), serotonin (5-hydroxytryptamine; 5-HT), dopamine (DA), and cathepsin D (CTSD) in the cerebellum have been evaluated.& nbsp; Results: The data showed that ACR induced redox disruptions as measured by increased MDA levels and inhibition of CAT, SOD, and GPx antioxidant enzyme activities. Besides, cerebellar monoamine neurotransmitters, 5HT and DA, were depleted in ACR-treated rats. Furthermore, ACR administration caused a significant elevation of CTSD activity, indicating that ACR could trigger apoptosis or apoptosis-like death. At the tissue level, cerebellar cortex sections from ACR-treated animals were characterized by severe neuronal damage. The administration of SIL to ACR-treated rats remarkably alleviated all the aforementioned ACR-induced effects.& nbsp; Conclusion: SIL has a potent therapeutic effect against ACR-induced cerebellar neurotoxicity in experimental rats via the attenuation of oxidative/antioxidative responses and the inhibition of CTSD-activity.
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