Comparison of the Protective Effects of Melatonin and Silymarin Against Gentamicin-Induced Nephrotoxicity in Rats

Ghaznavi, Habib; Mehrzadi, Saeed; Dormanesh, Banafsheh; Tabatabaei, Seyyed Mohammad; Vahedi, Habib; Hosseinzadeh, Azam; Pazoki‐Toroudi, Hamidreza; Rashidian, Amir

doi:10.1177/2156587215621672

Cited by 38 publications

(26 citation statements)

References 51 publications

(73 reference statements)

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“…Furthermore, MEL ameliorates nephropathy in diabetic rats’ kidneys via attenuation of oxidative stress . Also, there are other studies about the protective effects of melatonin in nephrotoxicity induced by cyclosporine, adriamycin, lead, ochratoxin and gentamicin and our results are entirely consistent with these studies .…”

Section: Discussionsupporting

confidence: 91%

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: 91%

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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“…SLY and NRG were dissolved in distilled water. Dosage of SLY and NRG were determined from those described by Ghaznavi et al (2015) and Sahu et al (2014), respectively.…”

Section: Chemicalsmentioning

confidence: 99%

Therapeutic effects of silymarin and naringin on methotrexate-induced nephrotoxicity in rats: Biochemical evaluation of anti-inflammatory, antiapoptotic, and antiautophagic properties

et al. 2017

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Silymarin (SLY) and naringin (NRG) are natural flavonoids that have been reported to have many benefits and medicinal properties. The present study was designed to investigate the protective effect of SLY and NRG against methotrexate (MTX)‐induced nephrotoxicity in experimental animals. Rats were subjected to oral pretreatment of SLY (25 and 50 mg/kg body weight (b.w.)/day) and NRG (50 and 100 mg/kg b.w./day) for 7 days against renal toxicity induced by single intraperitoneal administration of MTX (20 mg/kg b.w.). MTX resulted in an increase in serum toxicity markers, lipid peroxidation, and reduction in activities of antioxidant enzymes. Additionally, MTX provoked inflammatory responses by increasing the levels of TNF‐α, IL‐1β, IL‐6, NF‐κB, and activation of COX‐2 and iNOS. Furthermore, MTX administration caused apoptosis and autophagy by increasing activity of Caspase‐3 and light chain 3B level. Conversely, SLY and NRG therapy significantly decreased these values in rats. This study demonstrated that SLY and NRG protect against MTX‐induced nephrotoxicity. Practical applications Chemotherapeutic drugs have been used for cancer treatment for many years. However, in the treatment process, they may damage organs such as liver and kidney, prolong the treatment process and negatively affects patient welfare. This study revealed that silymarin and naringin exhibited potent anti‐inflammatory, antiapoptotic, and antiautophagic effect in renal injury caused by methotrexate, a chemotherapeutic drug. Therefore, treatment silymarin and naringin can be used for the beneficial effect against methotrexate‐induced kidney damage in cancer chemotherapy.

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“…[8][9][10][11] They remove reactive oxygen species (ROS) and reactive nitrogen species (RNS) 12,13 by radical scavenging and also by increasing the activity of antioxidant enzymes and expression of glutathione as an important endogenous antioxidant. [14][15][16][17] Via these actions, melatonin and its metabolites regulate a variety of molecular pathways such as inflammation, proliferation, apoptosis, and metastasis in different pathophysiological situations. [18][19][20][21][22]…”

Section: Introductionmentioning

confidence: 99%

Apoptosis signaling pathways in osteoarthritis and possible protective role of melatonin

Hosseinzadeh

Kamrava

Joghataei

et al. 2016

Journal of Pineal Research

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268

161

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Osteoarthritis (OA) is a degenerative joint disease characterized by progressive erosion of articular cartilage. As chondrocytes are the only cell type forming the articular cartilage, their gradual loss is the main cause of OA. There is a substantial body of published research that suggests reactive oxygen species (ROS) are major causative factors for chondrocyte damage and OA development. Oxidative stress elicited by ROS is capable of oxidizing and subsequently disrupting cartilage homeostasis, promoting catabolism via induction of cell death and damaging numerous components of the joint. IL-1β and TNF-α are crucial inflammatory factors that play pivotal roles in the pathogenesis of OA. In this process, the mitochondria are the major source of ROS production in cells, suggesting a role of mitochondrial dysfunction in this type of arthritis. This may also be promoted by inflammatory cytokines such as IL-1β and TNF-α which contribute to chondrocyte death. In patients with OA, the expression of endoplasmic reticulum (ER) stress-associated molecules is positively correlated with cartilage degeneration. Melatonin and its metabolites are broadspectrum antioxidants and free radical scavengers which regulate a variety of molecular pathways such as inflammation, proliferation, apoptosis, and metastasis in different pathophysiological situations. Herein, we review the effects of melatonin on OA, focusing on its ability to regulate apoptotic processes and ER and mitochondrial activity. We also evaluate likely protective effects of melatonin on OA pathogenesis. K E Y W O R D Sapoptosis, endoplasmic reticulum, inflammation, melatonin, mitochondria, molecular actions, osteoarthritis, oxidative stress

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Comparison of the Protective Effects of Melatonin and Silymarin Against Gentamicin-Induced Nephrotoxicity in Rats

Cited by 38 publications

References 51 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

Therapeutic effects of silymarin and naringin on methotrexate-induced nephrotoxicity in rats: Biochemical evaluation of anti-inflammatory, antiapoptotic, and antiautophagic properties

Apoptosis signaling pathways in osteoarthritis and possible protective role of melatonin

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