The protective properties of melatonin against aluminium‐induced neuronal injury

Al-Olayan, Ebtesam M.; El‐Khadragy, Manal F.; Moneim, Ahmed E. Abdel

doi:10.1111/iep.12122

Cited by 46 publications

(22 citation statements)

References 31 publications

(51 reference statements)

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“…MEL directly neutralizes ROS and NO as well as other toxic reactants. Also, MEL inhibits pro‐oxidative enzymes such as NO synthase, lipid peroxidation, MPO, COX‐2 and PC content . These data and our investigation clearly show that MEL might cause nephroprotection by decreasing the oxidative stress.…”

Section: Discussionsupporting

confidence: 75%

Pretreatment with melatonin protects against cyclophosphamide‐induced oxidative stress and renal damage in mice

Goudarzi

Khodayar

Tabatabaei

et al. 2017

Fundamemntal Clinical Pharma

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Cyclophosphamide (CP) is widely used in treatment of different cancers. Nephrotoxicity is one of the dose-limiting side effects of CP. This study was carried out to investigate the effect of melatonin (MEL) on CP-induced nephrotoxicity in mice. In this study, 50 Swiss albino mice (20-25 g) were randomly divided into five groups. Mice were pretreated with MEL intraperitoneally (i.p) in doses of 5, 10 and 20 mg/kg for five consecutive days, and CP (200 mg/kg, i.p) was administrated on the 5th day 1 h after the last dose of MEL. Then on day 6, blood samples were collected to determine serum creatinine (Cr) and blood urea nitrogen (BUN) levels. The kidneys were used for histological examination, biochemical assays and real-time PCR studies. Malondialdehyde (MDA), glutathione (GSH), protein carbonyl (PC), nitric oxide (NO) level, catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx) and myeloperoxidase (MPO) activity were assessed in renal tissue. In addition, the expression of SOD2 and PGx1 was measured using real-time PCR method in renal tissue. Results showed that CP administration significantly increases Cr, BUN, MDA, PC, NO level and MPO activity. It also decreases renal GSH level, SOD, GPx and CAT activity. Pretreatment with MEL (especially 20 mg/kg, i.p.) for 5 days prevented these changes; however, it did not affect the SOD activity. Our results revealed that MEL might be useful for prevention of the nephrotoxicity induced by CP through ameliorative effects on biochemical indices and oxidative stress parameters.

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Section: Discussionsupporting

confidence: 75%

Pretreatment with melatonin protects against cyclophosphamide‐induced oxidative stress and renal damage in mice

Goudarzi

Khodayar

Tabatabaei

et al. 2017

Fundamemntal Clinical Pharma

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“…MEL directly neutralizes ROS and NO as well as other toxic reactants. Also, MEL inhibits pro-oxidative enzymes such as NO synthase and lipid peroxidation [38,39]. In a recent study, it was shown that MEL attenuates oxidative stress of the retina in DR [40].…”

Section: Discussionmentioning

confidence: 99%

Protective effect of melatonin in the diabetic rat retina

Mehrzadi

Motevalian

Kanavi

et al. 2018

Fundamemntal Clinical Pharma

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Diabetic retinopathy (DR) is one of the most common and serious microvascular complications of diabetes. The aim of this study was to evaluate the effects of melatonin (MEL) on retinal injury in diabetic rats. In this study, 21 rats were randomly divided into three groups: control, diabetic, and diabetic + MEL. Streptozotocin was used to induce diabetes at a dose of 50 mg/kg, i.p., and blood glucose was measured to choose the diabetic rats for the study. MEL (20 mg/kg) was given orally for 7 weeks in diabetic rats starting 1 week after induction of diabetes. After 8 weeks, the groups were compared in terms of mean scores of fluorescein leakage, using fluorescein angiography. Reactive oxygen species (ROS) and malondialdehyde (MDA) levels were estimated in retina using commercially available assays. Structural changes in retinas were evaluated by light microscopy. Results showed that diabetes significantly increased the mean scores of fluorescein leakage, and MDA and ROS levels compared to control group. Treatment of the diabetic rats with MEL for 7 weeks prevented the alterations induced by diabetes in comparison with the diabetic control group.Based on these findings, it can be concluded that MEL might have beneficial effects in prevention of DR.

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“…Increased mitochondrial oxidative damage has also been observed in early pathological events leading to neurodegeneration (Beal, 1996). Aluminum-induced enhanced ROS production has been shown to cause DNA damage and finally apoptotic cell death (Alolayan et al, 2015). Protecting mitochondria from oxidative damage should be an effective therapeutic strategy against aluminum-induced oxidative stress and ensuing apoptosis.…”

Section: Introductionmentioning

confidence: 99%

The Protective Effect of DiDang Tang Against AlCl3-Induced Oxidative Stress and Apoptosis in PC12 Cells Through the Activation of SIRT1-Mediated Akt/Nrf2/HO-1 Pathway

et al. 2020

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Aluminum (Al) is considered a pathological factor for various neurological and neurodegenerative diseases, such as Alzheimer's disease (AD) and Parkinson's disease (PD). The neurotoxicity of aluminum can cause oxidative brain damage, trigger apoptosis, and ultimately cause irreversible damage to neurons. DiDang Tang (DDT), a classic formula within traditional Chinese medicine for promoting blood circulation and removing blood stasis and collaterals, is widely used for the treatment of stroke and AD. In this study, models of oxidative stress and apoptosis were established using AlCl 3 , and the effects of DDT were evaluated. We found that DDT treatment for 48 h significantly increased cell viability and reduced the release of lactate dehydrogenase (LDH) in AlCl 3induced PC12 cells. Moreover, DDT attenuated AlCl 3 -induced oxidative stress damage by increasing antioxidant activities and apoptosis through mitochondrial apoptotic pathways. Additionally, DDT treatment significantly activated the Sirtuin 1 (SIRT1) -mediated Akt/ nuclear factor E2 related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) pathways to limit AlCl 3mediated neurotoxicity. Our data indicated that DDT potently inhibited AlCl 3 -induced oxidative-stress damage and apoptosis in neural cells by activating the SIRT1-mediated Akt/Nrf2/HO-1 pathway, which provides further support for the beneficial effects of DDT on Al-induced neurotoxicity.

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The protective properties of melatonin against aluminium‐induced neuronal injury

Cited by 46 publications

References 31 publications

Pretreatment with melatonin protects against cyclophosphamide‐induced oxidative stress and renal damage in mice

Pretreatment with melatonin protects against cyclophosphamide‐induced oxidative stress and renal damage in mice

Protective effect of melatonin in the diabetic rat retina

The Protective Effect of DiDang Tang Against AlCl3-Induced Oxidative Stress and Apoptosis in PC12 Cells Through the Activation of SIRT1-Mediated Akt/Nrf2/HO-1 Pathway

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