Abstract
Renal ischemia-reperfusion (I/R) injury is a common but severe scientific problem. Luteolin has great anti-inflammatory and antioxidant effects. In this study, we studied the effect of luteolin on renal I/R injury in rats. Intragastric administration of luteolin or saline was performed in Sprague-Dawley rats before (40 mg/kg for three days) and after (one day) renal I/R modeling. Kidney and blood samples were harvested to detect the severity of renal injury 24 hours after operation. The results showed that luteolin-treated rats exhibited milder histomorphological changes with lower scores of renal histological lesions; lower blood urea nitrogen and creatinine levels; lower renal malondialdehyde (MDA), 8-oxo-deoxyguanosine (8-OHdG), and myeloperoxidase (MPO) levels; and higher superoxide dismutase (SOD) and catalase (CAT) activities in the kidney. Luteolin attenuated the increased levels of serum and renal tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6, renal high mobility group box-1 (HMGB1), and nuclear factor kappa β (NF-κB) expression levels in I/R rats. Furthermore, luteolin treatment significantly reduced renal cell apoptosis and endoplasmic reticulum (ER) stress caused by renal I/R injury. In conclusion, luteolin improved renal function in I/R rats by reducing oxidative stress, neutrophil infiltration, inflammation, renal cell apoptosis, and expression of HMGB1 and NF-κB, and ER stress.
Highlights
Renal ischemia-reperfusion (I/R) injury is mainly induced by surgery requiring clamping of the aorta, renovascular surgery, shock, trauma, and renal transplantation, which is the most frequent cause of acute kidney injury (AKI) [1, 2]
The renal injury scoring (I/R group versus I/R + luteolin group, 3.625 ± 0.2631 versus 2.375 ± 0.3750, P = 0 0163, Figure 2(b)) showed that luteolin treatment could significantly decrease the renal I/R injury, which was consistent with the hematoxylin and eosin (H&E) results
The results of the present study showed that luteolin could reverse the renal dysfunction, histological damages of renal injury, oxidative stress, neutrophil accumulation, inflammatory reaction, apoptosis, and endoplasmic reticulum stress during renal I/R injury in rats
Summary
Renal ischemia-reperfusion (I/R) injury is mainly induced by surgery requiring clamping of the aorta, renovascular surgery, shock, trauma, and renal transplantation, which is the most frequent cause of acute kidney injury (AKI) [1, 2]. In renal transplantation, the I/R damage could cause graft dysfunction and rejection, resulting in severe postoperative complications and death [3]. Despite many efforts have been done, the pathophysiology and exact mechanisms of I/R-induced renal injury are still not well illustrated. Dysfunction of tubular epithelial cells, microcirculatory disorders, robust inflammatory reaction, loss of endothelial integrity, activation of neutrophils, and release of reactive oxygen species (ROS) are generally accepted pathologic processes that all play important roles in I/R-induced renal injury. The methods applied for the attenuation of renal I/R injury include various anti-inflammatory and antioxidant drugs, endocrine hormones, erythropoietin, small interfering. It is important to explore new and effective methods to decrease renal I/R injury to solve this problem
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