Abstract
Background: The relationship between liver diseases and neurological defects is well established. Hepatic encephalopathy (HE) has been seen both in people with acute liver failure (ALF) and chronic liver disease (CLF). HE is a complex neuropsychiatric syndrome that is seen in patients suffering from liver dysfunction. Silymarin (Sm) has antioxidant, anti-inflammatory, and anti-carcinogenic features. In this study, the possible protective effects of silymarin were investigated against dorsolateral prefrontal cortex (DLPFC) damage induced by thioacetamide (TAA).
Method: To achieve this, male Sprague Dawley rats (200-250 g) were randomly divided into four groups, with 7 animals comprising each group: the control group, 50 mg/kg TAA group, 50 mg/kg Sm + TAA group, and 100 mg / kg Sm + TAA group.
Results: Differences between the groups were determined by performing immunohistochemical analysis of the PFC. Bax, TNF-α, and TUNEL expression increased in the brain tissue of the experimental group where only TAA was administered.
Conclusions: It was observed that in high doses in particular (100 mg/kg Sm + TAA group), Sm was effective in preventing PFC damage caused by TAA. It was determined that 100 mg/kg Sm significantly reduces TAA-induced inflammation (TNF-α and H&E) and apoptosis (Bax, TUNEL) in brain tissue.
Publisher
Granthaalayah Publications and Printers
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