Protective effects of melatonin against spinal cord injury induced oxidative damage in rat kidney: A morphological and biochemical study

Akakın, Dilek; Kiran, Demir; Özkan, Naziye; Erşahin, Mehmet; Ozdemir-Kumral, Zarife Nigar; Yeğen, Berrak Ç.; Şener, Göksel

doi:10.1016/j.acthis.2013.04.005

Cited by 18 publications

(8 citation statements)

References 37 publications

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“…It can also prevent cyclosporine ROS-induced renal functional impairment in rats without alteration in cyclosporine plasma levels (Akakin et al 2013;Malhotra et al 2004;Mun and Suh 2000;Şener et al 2002). The MT treatment has been demonstrated as a protection against GEN-induced nephrotoxicity that our results are entirely consistent with theirs (Lee et al 2012;Özbek et al 2000;Sener et al 2002;Shifow et al 2000).…”

Section: Discussionsupporting

confidence: 88%

Melatonin synergistically enhances protective effect of atorvastatin against gentamicin-induced nephrotoxicity in rat kidney

Mehrzadi

Kamrava

Dormanesh

et al. 2016

Can. J. Physiol. Pharmacol.

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The risk of serious side-effects such as nephrotoxicity is the principal limitation of gentamicin (GEN) therapeutic efficacy. Oxidative stress is considered to be an important mediator of GEN-induced nephrotoxicity. The present study was designed to evaluate the efficacy of the combination of melatonin (MT) plus atorvastatin (ATO) against GEN-induced nephrotoxicity in rats. We utilized 30 male Wistar albino rats allocated in 5 groups, each containing 6 rats: control, GEN (100 mg/kg/day), ATO (10 mg/kg/day) + GEN, MT (20 mg/kg/day) + GEN, and ATO (10 mg/kg/day) plus MT (20 mg/kg/day) + GEN. Kidney weight, serum creatinine and urea concentration, renal ROS, MDA, GSH levels, SOD, and CAT activity were determined. GEN-induced nephrotoxicity was evidenced by marked elevations in serum urea and creatinine, kidney weight, renal ROS, and MDA levels and reduction in renal GSH level, SOD and CAT activity. MT pretreatment significantly lowered the elevated serum creatinine concentration, kidney weight, renal ROS and MDA levels. However ATO could not reduce these parameters, but similarly to MT, it was able to enhance the renal GSH level, CAT and SOD activity. In addition, a combination therapy of MT plus ATO enhanced the beneficial effects of ATO, while not changing the effects of MT effects or even improving them. The present study indicates that a combination therapy of MT plus ATO can attenuate renal injury in rats treated with GEN, possibly by reducing oxidative stress, and it seems that MT can enhance the beneficial effects of ATO.

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Section: Discussionsupporting

confidence: 88%

Melatonin synergistically enhances protective effect of atorvastatin against gentamicin-induced nephrotoxicity in rat kidney

Mehrzadi

Kamrava

Dormanesh

et al. 2016

Can. J. Physiol. Pharmacol.

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“…Upon exposure to unconjugated bilirubin, release of pro‐inflammatory cytokines occurs from astrocytes and microglia, as well as from migrated neutrophils . In accordance with our previous studies, which demonstrate that melatonin alleviates oxidative stress and exerts neuroprotection by inhibiting neutrophil infiltration , the current findings also verified that the inhibitory effect of melatonin on neutrophil infiltration participates in its neuroprotective effect against bilirubin neurotoxicity. In addition to its action as an antioxidant and as an MPO inhibitor, melatonin might be providing neuroprotection by inhibiting hypochloric acid‐mediated heme destruction of hemoproteins and subsequent free iron release in the present hemolysis‐induced bilirubin neurotoxicity.…”

Section: Discussionsupporting

confidence: 91%

The neuroprotective and anti‐apoptotic effects of melatonin on hemolytic hyperbilirubinemia‐induced oxidative brain damage

Pazar

Kolgazi

Memişoğlu

et al. 2015

Journal of Pineal Research

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Melatonin exerts protection in several inflammatory and neurodegenerative disorders. To investigate the neuroprotective effects of melatonin in an experimental hemolysis-induced hyperbilirubinemia, newborn Sprague-Dawley rats (25-40 g, n = 72) were injected with phenylhydrazine hydrochloride (PHZ; 75 mg/kg) and the injections were repeated at the 24th hour. Rats were treated with saline or melatonin (10 mg/kg) 30 min before the first and second PHZ injections and 24 h after the 2nd PHZ injections. Control rats (n = 24) were injected with saline, but not PHZ. At sixth hours after the last injections of saline or melatonin, all rats were decapitated. Tumor necrosis factor (TNF)-α, IL-1β, IL-10 and brain-derived neurotrophic factor (BDNF) and S100B levels in the plasma were measured. Brain tissue malondialdehyde (MDA), glutathione (GSH) levels and myeloperoxidase (MPO) activities were measured, and brain tissues were evaluated for apoptosis by TUNEL method. In the saline-treated PHZ group, hemoglobin, hematocrit levels were reduced, and total/direct bilirubin levels were elevated when compared to control group. Increased plasma TNF-α, IL-1β levels, along with decreased BDNF, S100B and IL-10 values were observed in the saline-treated PHZ group, while these changes were all reversed in the melatonin-treated group. Increased MDA levels and MPO activities in the brain tissues of saline-treated hyperbilirubinemic rats, concomitant with depleted brain GSH stores, were also reversed in the melatonin-treated hyperbilirubinemic rats. Increased TUNEL(+) cells in the hippocampus of saline-treated PHZ group were reduced by melatonin treatment. Melatonin exerts neuroprotective and anti-apoptotic effects on the oxidative neuronal damage of the newborn rats with hemolysis and hyperbilirubinemia.

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“…Oxygen radicals released from neutrophils are toxic to the cell membrane component , and free radical‐induced lipid peroxidation is important in the autodestruction of the injured spinal cord. Previously research suggested not only the protection conferred by melatonin on oxidative damage, but also its ability to reduce neutrophil‐induced toxicity . Although injection of melatonin after SCI has been shown to reduce thiobarbituric acid‐reactive substance content and myeloperoxidase activity, as well as facilitate recovery of the damaged spinal cord, it has not been shown to promote regeneration of nerve cells.…”

Section: Introductionmentioning

confidence: 99%

Combination of melatonin and Wnt‐4 promotes neural cell differentiation in bovine amniotic epithelial cells and recovery from spinal cord injury

Gao

Bai

Zheng

et al. 2016

Journal of Pineal Research

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Although melatonin has been shown to exhibit a wide variety of biological functions, its effects on promoting differentiation of neural cells remain unknown. Wnt signaling mediates major developmental processes during embryogenesis and regulates maintenance, self-renewal, and differentiation of adult mammalian stem cells. However, the role of the noncanonical Wnt pathway during neurogenesis remains poorly understood. In this study, the amniotic epithelial cells ( AECs) were isolated from bovine amnion and incubated with various melatonin concentrations (0.01, 0.1, 1, 10, or 100 μm) and 5 × 10(-5) m all-trans retinoic acid (RA) for screening optimum culture medium of neural differentiation, compared with each groups, 1 μm melatonin and 5 × 10(-5) m RA were selected to induce neural differentiation of AECs, and then siMT1, siMT2, oWnt-4, and siWnt-4 were expressed in AECs to research role of these genes in neural differentiation. Efficiency of neural differentiation was evaluated after expressed above genes using flow cytometry. Cell function of neural cells was demonstrated in vivo using spinal cord injury model after cell transplantation, and damage repair of spinal cord was assessed using cell tracking and Basso, Beattie, Bresnahan Locomotor Rating Scale scores. Results demonstrated that melatonin stimulated melatonin receptor 1, which subsequently increased bovine amniotic epithelial cell vitality and promoted differentiation into neural cells. This took place through cooperation with Wnt-4. Additionally, following cotreatment with melatonin and Wnt-4, neurogenesis gene expression was significantly altered. Furthermore, single inhibition of melatonin receptor 1 or Wnt-4 expression decreased expression of neurogenesis-related genes, and bovine amniotic epithelial cell-derived neural cells were successfully colonized into injured spinal cord, which suggested participation in tissue repair.

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Protective effects of melatonin against spinal cord injury induced oxidative damage in rat kidney: A morphological and biochemical study

Cited by 18 publications

References 37 publications

Melatonin synergistically enhances protective effect of atorvastatin against gentamicin-induced nephrotoxicity in rat kidney

Melatonin synergistically enhances protective effect of atorvastatin against gentamicin-induced nephrotoxicity in rat kidney

The neuroprotective and anti‐apoptotic effects of melatonin on hemolytic hyperbilirubinemia‐induced oxidative brain damage

Combination of melatonin and Wnt‐4 promotes neural cell differentiation in bovine amniotic epithelial cells and recovery from spinal cord injury

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