Aqueous Extract from Cinnamomum zeylanicum (Lauraceae) Stem Bark Ameliorates Gentamicin-Induced Nephrotoxicity in Rats by Modulating Oxidative Stress and Inflammatory Markers

Abstract

Nephropathies and especially nephrotoxicity have become one of the serious causes of life-threatening conditions because of intensive exposure to xenobiotic whether by environmental pollution or by drug abuse. The present study was undertaken to assess the protective effects of Cinnamomum zeylanicum stem bark aqueous extract (AECZ) on gentamicin-induced nephrotoxicity. AECZ was prepared by maceration in water and tested orally at the doses of 200 and 400 mg/kg/day to prevent gentamicin-induced nephropathies in male Wistar rats. Gentamicin (100 mg/kg/day) was administered for 14 consecutive days by intraperitoneal route, concomitantly with AECZ or silymarin (50 mg/kg/day) used as reference drug. Animal body weight was monitored during the treatment. After the last treatment on the 14th day, animals were sacrificed. Blood was collected for the evaluation of hematological and renal function biomarkers. The homogenate of one kidney was used to assess oxidative stress markers and proinflammatory cytokines, while the other one was fixed in formaldehyde for histopathological studies. Gentamicin decreased body weight, serum total proteins, and calcium level but increased kidneys’ relative weight, serum creatinine, urea, and uric acid. Moreover, the levels of reduced glutathione, catalase, and superoxide dismutase activities were decreased, while an increase in malondialdehyde, proinflammatory cytokines (TNF-α, IL-1β, and IL-6), and nitrites was observed in the negative control group as compared to normal control. Histological analysis of the kidney revealed the presence of tubular necrosis, glomerular degeneration, and macrophage infiltration in the gentamicin-treated group. All these impairment parameters were prevented by AECZ and silymarin treatments. AECZ has a protective effect against gentamicin-induced nephrotoxicity. The antioxidant and anti-inflammatory potentials of this extract may highly contribute to its nephroprotective activity.

Effect of Vitellaria paradoxa (Shea Butter) Rich Diet on Gentamicin Induced Nephrotoxicity in White Wistar Rats

“…Tubular cytotoxicity is the result of many interconnected actions, triggered by drug accumulation in epithelial tubular cells [31]. Results of the study corroborate the findings of Quiros et al, in which a significant nephrotoxic effect of gentamicin, administered at a dose of 80 mg/kg body weight, was observed in other animal species [31]. The amelioration of gentamicin induced nephrotoxicity by Shea butter rich diet, as seen in this, study was dose dependent.…”

“…The exact mechanism by which gentamicin induces nephrotoxicity is unknown. Tubular cytotoxicity is the result of many interconnected actions, triggered by drug accumulation in epithelial tubular cells [31]. Results of the study corroborate the findings of Quiros et al, in which a significant nephrotoxic effect of gentamicin, administered at a dose of 80 mg/kg body weight, was observed in other animal species [31].…”

Crocus sativus L. Stigmas, Tepals, and Leaves Ameliorate Gentamicin-Induced Renal Toxicity: A Biochemical and Histopathological Study

“…An inflammatory response and renal edema may be to blame for the considerable rise in the relative kidney weight seen in the group treated with gentamicin. [ 23 ]. This was confirmed by histological sections, which showed apparent renal tubular swelling ( Figure 1 ).…”

Antioxidant and anti-apoptotic roles of sesame oil and N acetylcysteine against gentamicin-induced nephrotoxicity in rats

“…Accumulation of GM in epithelial cells of the kidney exerted cell death through free radical generation, lowered blood flow to the kidney, and induced inflammation (Sharma et al 2021). The severity of GM-induced nephrotoxicity is promoted by oxidative stress (Abdeen et al 2021;Atsamo et al 2021). GM elicited a rise in MDA, a decline in SOD activity, and GSH content (Atsamo et al 2021;Elkomy et al 2019).…”