Protective effect of hydroalcoholic extract of <i>Pistacia vera</i> against gentamicin-induced nephrotoxicity in rats

Ehsani, Vahid; Amirteimoury, Morteza; Taghipour, Zahra; Shamsizadeh, Ali; Bazmandegan, Gholamreza; Rahnama, Amir; Khajehasani, Fatemeh; Fatemi, Iman

doi:10.1080/0886022x.2017.1326384

Cited by 33 publications

(19 citation statements)

References 29 publications

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“…Consistent with biochemical assessment, renal histopathological results demonstrate structural changes in renal tissue of CP‐treated rats. We showed that administration of CP at the dose 200 mg/kg causes histopathological lesions in kidney like hemorrhage, tubular degeneration and leukocyte cell infiltration tubular and these findings are in agreement with the previous studies . Inflammation could directly cause renal damage and promote kidney cell death via the production of ROS during inflammatory processes .…”

Section: Discussionsupporting

confidence: 92%

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: 92%

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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“…Gentamicin-induced nephrotoxicity at the beginning of the development of the pathological process is characterized by the development of oliguric form of renal failure, accompanied by retention azotemia, proteinuria, increased loss of sodium and potassium ions with urine, resulting in hypokalemia (Table 1), which reflects the significant damage and death of proximal tubular cells along with injury of glomeruli, and corresponds to the results of similar experimental studies of other authors [1, 4, 8-12, 17, 18]. According to the obtained results of the morphological examination, histopathological changes, namely the necrosis and degeneration of the proximal tubular epithelial cells in the form of vacuolization and hydropic dystrophy, and glomerular damage ( Figure 2) were revealed for gentamicin nephropathy [3,[8][9][10][11][12]14]. It is known that the most important mechanism of gentamicin nephrotoxicity is the hyperproduction of reactive oxygen species, causing damage to proteins, DNA and peroxidation of lipids, with an alteration of the integrity of cellular membranes and development of morphofunctional disorders [1,17].…”

Section: Discussionsupporting

confidence: 87%

“…It is known that the most important mechanism of gentamicin nephrotoxicity is the hyperproduction of reactive oxygen species, causing damage to proteins, DNA and peroxidation of lipids, with an alteration of the integrity of cellular membranes and development of morphofunctional disorders [1,17]. This fact conditions numerous research on the effectiveness of prevention of the gentamicin nephropathy, using known and new antioxidants [1,2,4,[8][9][10][11][12]20].…”

Section: Discussionmentioning

confidence: 99%

“…At that, the maintenance of glomerular filtration may be explained by the direct antioxidant activity of the drug, since reactive oxygen species and nitrogen oxides directly lead to a decrease in GFR [16]. The established renal effects of melatonin in toxic kidney damage correspond to the criteria of nephroprotective action under the conditions of AKI development [2,[8][9][10][11][12].…”

Section: Discussionmentioning

confidence: 99%

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Morphofunctional Changes in Kidneys of Rats With Gentamicin-Induced Acute Kidney Injury and Use of Melatonin

et al. 2018

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Aminoglycosides are effective antibiotics, but their accumulation in kidney cortex causes nephrotoxic effects in 20-30% of patients, which significantly limits their use. For this reason, search for the new therapies aimed at prevention of gentamicin-induced acute kidney injury (AKI) is highly relevant. Thus, the objective of our research was to study the functional and histopathological changes in kidneys of rats with gentamicin-induced AKI, and estimate the renoprotective potential of pineal hormone melatonin, which possesses antioxidant, anti-inflammatory and immunomodulatory effects. The study was conducted on 24 non-linear male rats. Gentamicin-induced AKI was modeled by daily administration of 4% gentamicin sulphate (80 mg/kg) for 6 days. Melatonin (Sigma Aldrich, USA) was injected daily at a dose of 5 mg/kg. Functional state of kidneys was assessed by diuresis, creatinine clearance, urine protein excretion, fractional excretion of sodium, and plasma potassium level. Documentation of the pathological processes was performed by the computer morphometry of objects in histological preparations. Statistical analysis of the data was performed using SPSS 17.0 software. Administration of gentamicin resulted in a significant impairment of renal function of experimental animals. A decrease in creatinine clearance by 3.1 times along with a reduction of diuresis by 1.9 times, and an increase in plasma creatinine concentration by 2.6 times was observed. There also was an increase in urine protein level by 5.2 times, an elevation of fractional sodium excretion and a reduction of plasma potassium level. Use of melatonin caused a significant improvement of renal function comparing to model pathology group. Functional disturbances were accompanied with the significant histopathological changes in kidney tissue: necrosis of the 27±5.2% epithelial cells of proximal tubules with the signs of hydropic vacuolization (7±2.1%) or reversible hydropic swelling (76±1.5%) in the rest of cells; swelling or deformation of some glomeruli. In the medulla tubular lumen were dilated and partially filled with hyaline casts, tubular cells had signs of dystrophy. Use of melatonin contributed to the restraint of the histopathological changes, confirmed by the decrease of the prevalence and severity of tubular necrosis (1.2%), dystrophy (64±2.3%), and injury of glomeruli. Obtained results verify the significant nephroprotective effect of pineal hormone melatonin, providing a background for the further in-depth study of its renal effects as well as its prospects as a nephroprotector.

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“…Moreover, it has been shown that administration of Cisplatin (CP) or CP + Cerium oxide nanoparticles (CeO2 NPs) in rats increased the water intake and urine volume compared with saline, indicated that the damaged renal tubules could cause the deterioration of capacity of tubular cells to reabsorb water, and subsequent polyuria leading to dehydration (Nemmar et al, 2019). Similarly, the increase of urine volume was one of the nephrotoxicity characteristics in an acute renal failure (ARF) rat model induced by gentamicin in a study about plant extracts for the prevention and attenuation of ARF (Ehsani et al, 2017). These results suggested that the physiological functions of the kidney were damaged, resulting in an imbalance of hydration state after exposure to PM 2.5 .…”

Section: Discussionmentioning

confidence: 93%

PM2.5 exposure induced renal injury via the activation of the autophagic pathway in the rat and HK-2 cell

Huang

Zhou

Liu

et al. 2020

Preprint

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Abstract Background: Exposure to airborne fine particulate matter (PM2.5) has been declared to be harmful to human kidney. However, whether activation of the autophagic pathway plays key roles in the nephrotoxicity caused by PM2.5 exposure is still poorly understood. The aim of this study was to explore the mechanism of kidney damage after PM2.5 exposure in vivo and in vitro.Results: In the present study, statistically significant alterations in water intake, urine flow rate and mean blood pressure were observed between the concentrated PM2.5 (PM2.5) group and the filtered air (FA) group. Exposed animals showed severe edema of renal tubular epithelial cells, capillary congestion, reduction of the glomerular urinary space and early pro-fibrotic state. Moreover, significant increases in the levels of early kidney damage markers were observed in the exposed rats and these animals exhibited more apoptosis rate in kidney cells. In addition, PM2.5 exposure activated the autophagic pathway, as evidenced by LC3-I to LC3-II conversion, activation of P62 and beclin-1. All of these effects are in concurrence with the presence of more autophagosomes both in vivo and in vitro after PM2.5 exposure. Conclusions: Taken together, our findings indicated that PM2.5-induced renal function impairment via the activation of the autophagic pathway in renal tubular epithelial cells.

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Protective effect of hydroalcoholic extract of Pistacia vera against gentamicin-induced nephrotoxicity in rats

Cited by 33 publications

References 29 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

Morphofunctional Changes in Kidneys of Rats With Gentamicin-Induced Acute Kidney Injury and Use of Melatonin

PM2.5 exposure induced renal injury via the activation of the autophagic pathway in the rat and HK-2 cell

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