Toll-like receptor-2 mediates systemic inflammation in gentamicin-induced rat nephrotoxicity.

Toll-like receptor-2 mediates systemic inflammation in gentamicin-induced rat nephrotoxicity. Clin Exp Pharmacol Physiol. 2020 May 08;: Authors: Karimi Z, Pakfetrat Z, Roozbeh J, Janfeshan S Abstract Gentamicin is an aminoglycoside antibiotic commonly administrated to patients with gram-negative infections. Gentamicin induced nephrotoxicity by functional and structural impairment. Toll like receptors (TLRs) as key mediators in the innate and adaptive immune system response involved in gentamicin induced-nephrotoxicity. The present study aimed to investigate the gene expression of TLR2 and pro-inflammatory cytokines in the renal tissues and buffy coat of the whole blood in gentamicin treated rats. Twenty adult male Sprague Dawley rats weighting 180-200 were randomly divided into gentamicin (100 mg/kg, i.p) and control groups (n=10). After 10 days, the serum creatinine (Cr) levels and blood urea nitrogen (BUN) were measured. The mRNA levels of TLR2, TNF-α, IL-1β, and MCP-1 were investigated in the renal tissue and buffy coat by qRT-PCR. Kidney histological analysis performed by hematoxylin-eosin (H&E) staining. Functional disturbance is characterized by a significant increase in the serum levels of Cr and BUN in the gentamicin group. Renal tissue slides of the gentamicin group indicated severe glomerular and tubular damages including lobulation of the glomerular tuft, Bowman's space enlargement, acute tubular necrosis, and proxim...
Source: Clinical and Experimental Pharmacology and Physiology - Category: Drugs & Pharmacology Authors: Tags: Clin Exp Pharmacol Physiol Source Type: research