Myrtenal Pretreatment Exerts a Protective Effect Against Renal Ischemia‐Reperfusion Injury in Rats

Acute kidney injury (AKI) is a serious condition with high mortality in intensive care units and during vascular surgeries. Renal ischemia-reperfusion injury (IRI) significantly contributes to AKI. Preclinical studies have shown that myrtenal (Myrt) has anti-inflammatory and antioxidant properties. We hypothesized that Myrt might alleviate renal damage caused by IRI through the modulation of oxidative stress and inflammatory processes. This study aimed to investigate the renoprotective potential of Myrt against IRI using biochemical evaluations and histological examinations. Forty male Sprague Dawley rats were assigned to four groups: sham, IRI, Myrt40+IRI, and Myrt80+IRI. Animals received daily intraperitoneal injections of Myrt (40-80 mg/kg) or solvent for 9 days before surgery. The sham group underwent laparotomy, while the other groups had AKI induced via bilateral renal pedicle clamping for 45 min, followed by 24 h of reperfusion. Renal function was assessed by blood urea nitrogen (BUN), creatinine, kidney injury molecule-1 (KIM-1) and neutrophil gelatinase-associated lipocalin (NGAL) levels. Inflammatory markers interleukin-1 beta (IL-1β), tumor necrosis factor-alpha (TNF-α) were measured, along with oxidative stress parameters malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH). Renal damage was evaluated histopathologically using hematoxylin and eosin staining and apoptosis was assessed via caspase-3 immunohistochemistry. In the IRI group, serum BUN and creatinine levels were significantly higher than the sham group but were reduced by Myrt pretreatment (p < 0.05). IRI also led to significant increases in MDA, KIM-1, NGAL, IL-1β, and TNF-α in kidney tissue (p < 0.05), which were notably decreased by Myrt pretreatment (p < 0.05). Myrt also restored SOD and CAT enzyme activities and GSH levels reduced by IRI (p < 0.05). Histological analysis showed Myrt significantly alleviated renal tissue damage and reduced caspase-3 immunoreactivity due to IRI (p < 0.05). The findings suggest that Myrt has a protective effect against renal IRI.

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Publication Details

Journal
Journal of Biochemical and Molecular Toxicology
Published
2025-03-01
DOI
https://doi.org/10.1002/jbt.70202
Citations
4
Primary Topic
Acute Kidney Injury Research
Type
article
Field-Weighted Citation Impact
5.72
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article

Myrtenal Pretreatment Exerts a Protective Effect Against Renal Ischemia‐Reperfusion Injury in Rats

Aslı Çetin, Suat Tekin, Evren Köse, Engin Korkmaz et al.
4 citations
Journal of Biochemical and Molecular Toxicology
Acute Kidney Injury Research
5.72
article

Myrtenal Pretreatment Exerts a Protective Effect Against Renal Ischemia‐Reperfusion Injury in Rats

Aslı Çetin, Suat Tekin, Evren Köse, Engin Korkmaz, Leyla Beytur
article en
4 citations

Abstract

Acute kidney injury (AKI) is a serious condition with high mortality in intensive care units and during vascular surgeries. Renal ischemia-reperfusion injury (IRI) significantly contributes to AKI. Preclinical studies have shown that myrtenal (Myrt) has anti-inflammatory and antioxidant properties. We hypothesized that Myrt might alleviate renal damage caused by IRI through the modulation of oxidative stress and inflammatory processes. This study aimed to investigate the renoprotective potential of Myrt against IRI using biochemical evaluations and histological examinations. Forty male Sprague Dawley rats were assigned to four groups: sham, IRI, Myrt40+IRI, and Myrt80+IRI. Animals received daily intraperitoneal injections of Myrt (40-80 mg/kg) or solvent for 9 days before surgery. The sham group underwent laparotomy, while the other groups had AKI induced via bilateral renal pedicle clamping for 45 min, followed by 24 h of reperfusion. Renal function was assessed by blood urea nitrogen (BUN), creatinine, kidney injury molecule-1 (KIM-1) and neutrophil gelatinase-associated lipocalin (NGAL) levels. Inflammatory markers interleukin-1 beta (IL-1β), tumor necrosis factor-alpha (TNF-α) were measured, along with oxidative stress parameters malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH). Renal damage was evaluated histopathologically using hematoxylin and eosin staining and apoptosis was assessed via caspase-3 immunohistochemistry. In the IRI group, serum BUN and creatinine levels were significantly higher than the sham group but were reduced by Myrt pretreatment (p < 0.05). IRI also led to significant increases in MDA, KIM-1, NGAL, IL-1β, and TNF-α in kidney tissue (p < 0.05), which were notably decreased by Myrt pretreatment (p < 0.05). Myrt also restored SOD and CAT enzyme activities and GSH levels reduced by IRI (p < 0.05). Histological analysis showed Myrt significantly alleviated renal tissue damage and reduced caspase-3 immunoreactivity due to IRI (p < 0.05). The findings suggest that Myrt has a protective effect against renal IRI.

Journal of Biochemical and Molecular ToxicologyVol. 39(3)
Inonu University (TR)
Openalex Percentile: Top 4%
Acute Kidney Injury Research
5.72
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