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Abstract Title:

Ameliorative effects of corn silk extract on acetaminophen-induced renal toxicity in rats.

Abstract Source:

Environ Sci Pollut Res Int. 2021 Jan ;28(2):1762-1774. Epub 2020 Aug 27. PMID: 32856245

Abstract Author(s):

Enas M Wans, Mohamed M Ahmed, Ahmed A Mousa, Enas A Tahoun, Sahar H Orabi

Article Affiliation:

Enas M Wans

Abstract:

The current study aimed to investigate the protective effect of corn silk methanolic extract (CSME) against acetaminophen (APAP)-induced nephrotoxicity. The present study was carried out on 40 male Wistar albino rats, which were randomly divided into four groups (n = 10): control group, orally administered with a single dose of 1.8 ml 0.9% normal saline at the last day of the experiment; CSME group, orally received CSME (400 mg/kg BW daily for 5 weeks); APAP group, orally administered with a single dose of APAP (2 g/kg BW); and CSME and APAP group, orally administered with CSME, followed by a single oral dose of APAP. The results of this study revealed that APAP caused a significant increase in serum urea, creatinine concentrations, and malondialdehyde (MDA) concentrations in renal tissues. In addition, APAP caused a significant decrease in superoxide dismutase (SOD) and glutathione peroxidase (GPX) activities in renal tissues compared with the control group. Furthermore, APAP caused marked renal damage as revealed by alterations in histopathological architectures of kidney tissues. APAP resulted in a marked expression of caspase 3 and nuclear factor κB (NFĸβ) within the renal tubules, while caused marked decrease of proliferating cell nuclear antigen (PCNA) immunostaining and transforming growth factor beta 1 (TGFβ 1) expression within the epithelial lining of the renal tubules. However, pre-treatment with CSME returned all biochemical parameters, histopathological changes, and immunohistochemical parameters toward normal levels as the control group. In conclusion, oral administration of CSME protected rats against APAP renal toxicity through its antioxidant, anti-apoptotic, and anti-inflammatory protective mechanisms.

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