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Fimasartan ameliorates renal ischemia reperfusion injury via modulation of oxidative stress, inflammatory and apoptotic cascades in a rat model
Abstract
It is told about the effect of ARBs, fimasartan, as a protective agent against AKI due to IRI.
... IRI is considered as one of the principle causes of injury in the organs, especially in the kidneys [18]. AKI is a multi-etiological global public health issue with no definitive pharmacological treatment. ...
... During renal IRI, mitochondrial respiratory chain burst of ROS and subsequent excessive rise of ROS, along with lack of activity of anti-oxidative factors such as glutathione peroxidase, catalase and SOD can lead to substantial damage to major biomolecules including DNA, proteins and lipids which in turn leads to cell death and apoptosis afterwards [18]. As mentioned before, one of the important mechanisms in damage caused by IRI is attributed to the role of inflammatory pathways. ...
... There are several studies investigating effects of different agents on ischemia/reperfusion induced renal injury [18,[28][29][30]. many of these agents, however, seem to have limitations when it comes to clinical application. ...
Background
Renal ischemia reperfusion injury (IRI) is a post‐ischemic event, which can lead to subsequent acute kidney injury (AKI), transplant failure, renal dysfunction and fibrosis via heightened oxidative stress and production of inflammatory cytokines and chemokines.
Objective
This study aims to assess the effect of Modafinil, a wake‐promoting agent with previously proven anti‐inflammatory and anti‐oxidative properties, on ameliorating renal IRI.
Methods
A total of 30 male Wistar rats were divided into five groups: Sham‐operated group, ischemia reperfusion (I/R) control group and Modafinil pre‐treated groups (at different doses of 50, 100 and 150 mg/kg). IRI was induced by means of bilaterally clamping the renal arteries for 45 min, followed by 24 h of reperfusion.
Results
Tissue pathological assessments demonstrated a reduction of glomerular, vascular and interstitial injury at doses of 50 and 100 mg/kg of Modafinil. The biochemical studies showed a significant decrease in tissue pro‐inflammatory factors, including tumor necrosis factor alpha (TNF‐α), Interleukin‐18 (IL‐18) and lactate dehydrogenase (LDH). Moreover, an elevation was observed in levels of super oxide dismutase (SOD) and catalase, indicating the reduction of oxidative stress. Furthermore, the levels of creatinine (Cr), urea and neutrophil gelatinase‐associated lipocalin (NGAL) were declined, indicating the improvement in renal function at effective doses of Modafinil (50 and 100 mg/kg) compared to the I/R control group without Modafinil pre‐treatment.
Conclusion
Our findings suggest that Modafinil holds promise as an effective therapeutic agent to address the clinical challenges associated with kidney IRI reducing the need for hospitalization and potentially alleviating related morbidities.
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