Mechanism of grape seeds extract protection against paracetamol renal cortical damage in male Albino rats

Abstract

OBJECTIVE: The aim of the study was to assess the possible protective role of grape seeds extract (GSE) in ameliorating the toxic effects of paracetamol overdose on the rat renal cortical tissue. BACKGROUND: Paracetamol is one of the widely used non-steroidal anti-inflammatory drugs (NSAIDs). Unfortunately, it was reported as the most common cause of toxic ingestion in the world. Grape seeds extract (GSE) is known to have a strong antioxidant and anti-inflammatory properties. METHODS: The rats were divided into 4 groups; control group, GSE group, paracetamol group and GSE with paracetamol group. Kidney specimens were processed for biochemical, histological and immunohisto-chemical studies. RESULTS: The study showed marked biological changes in the form of significant increase in serum urea and creatinine levels with significant decrease in renal superoxide dismutase with paracetamol group. Furthermore, Proximal (PCT) and distal convoluted tubules showed marked degeneration, dense nuclear staining, cytoplasmic vacuolization, and partial loss of the brush borders. Most tubules were dilated, irregular and were filled with hyaline casts. PCT and DCT showed less PAS reaction and more COX-2 and caspase expression if compared with the control and the GSE groups. Concomitant administration of grape seeds extract with paracetamol revealed a noticeable amelioration of these biochemical and histological changes. Proximal and distal convoluted tubules showed less PAS reaction and more COX2 and caspase expression if compared with the control and the GSE. Concomitant administration of GSE with paracetamol revealed a noticeable amelioration of these biochemical and histological changes. CONCLUSION: Grape seeds extract provided biochemical and histo-pathological improvement in paracetamol induced renal cortical toxicity. These findings revealed that this improvement was associated with a decrease in oxidative damage and apoptosis.