Effects of melatonin on the serum levels of pro-inflammatory cytokines and tissue injury after renal ischemia reperfusion in rats

Abstract

We investigated the changes in the serum levels of tumor necrosis factor (TNF)-a and interleukin (IL)-6, the pro-inflammatory cytokines, and the possible effect of melatonin on the modulation of these inflammatory molecules after renal ischemia reperfusion (IR). The study was carried out in the laboratory of Department of Pharmacology. Forty-six male Wistar albino rats were divided into five groups as control (n ¼ 6), positive control (n ¼ 4), sham (n ¼ 12), renal IR (n ¼ 12), and renal IR melatonin (n ¼ 12). After 1 h renal pedicle occlusion, the blood samples were taken for the measurement of cytokine levels at second hour of the reperfusion. The rats were sacrificed after 24 h of reperfusion for histopathological evaluation. Melatonin or vehicle was administrated to IR rats. Lipopolysaccharide (LPS) was administered to the positive control group and the blood was taken at fourth hour. Serum TNF-a levels increased significantly in renal IR and LPS groups. Serum IL-6 levels were not different from control except the LPS group. There was no significant correlation between the serum TNF-a levels and the histopathological score after renal IR. Melatonin treatment reversed the increase of serum TNF-a levels and histopathological injury in renal tissue after renal IR. Melatonin may have a protective effect by reducing the serum level of TNF-a in renal IR.

Rutaecarpine alleviates renal ischemia reperfusion injury in rats by suppressing the JNK/p38 MAPK signaling pathway and interfering with the oxidative stress response

“…Rutaecarpine treatment inhibits the production of inflammatory cytokines in renal tissue. The inflammatory cytokines secreted by renal endothelial cells and parenchymal cells are important markers of the inflammatory response following IRI (30). As shown in Table III, when compared with the sham group, levels of the inflammatory cytokines NF-κB, TNF-α, IL-6 and ICAM-1 increased in the renal tissues of rats in the IRI, NS, Ru-30 and Ru-60 groups (P<0.05) compared with the sham group, indicating that inflammatory factors were released from the renal tissue during the early stage of IRI.…”

Effects of Lycopene Alone or Combined with Melatonin on Methotrexate-Induced Nephrotoxicity in Rats

“…In several animal models of chronic kidney disease, involving experimental hypertension, diabetes mellitus and various models of nephrotoxicity (Hrenak et al, 2015). Mel treatment reversed the increase of serum TNF-α levels and histopathological injury in renal tissue after renal IR (Oguz et al, 2015). Mel, with a dose of 40 mg/kg, has the potential to reduce MTX induced oxidative stress, neutrophil infiltration as well as renal damage (Abraham et al, 2010).…”

“…Chronic Mel treatment reduces renal injury by reducing lipid oxidation and NO production in STZ-induced diabetic rats exposed to IR (Kurcer et al, 2007). In our previous study we found that Mel treatment reversed the increase of serum tumor necrosis factor-alpha (TNF-α) levels and histopathological injury in renal tissue after renal IR (Oguz et al, 2015). It has been reported that Mel has the potential to reduce MTX induced oxidative stress, neutrophil infiltration as well as renal damage at a dose of 40 mg/kg in rats (Abraham, 2010).…”

Apoptosis and Histopathology of the Heart after Renal Ischemia-Reperfusion in Male Rat Running title: Ischemia-Reperfusion Injury

“…This connection of inflammatory cytokines in renal IRI-induced remote organ dysfunction has been corroborated by critical roles of cytokines in modulating the remote organ lung effects during AKI (21). Serum pro-inflammatory cytokines such as TNF-α levels increase significantly in renal IR (22). These circulatory inflammatory cytokines transferred to other organs such as lung (9) and probably heart, that may cause apoptosis in this tissues.…”