scholarly journals Cisplatin Nephrotoxicity and Protection by Milk Thistle Extract in Rats

2005 ◽  
Vol 2 (3) ◽  
pp. 383-386 ◽  
Author(s):  
Gholamreza Karimi ◽  
Mohammad Ramezani ◽  
Zahra Tahoonian
Keyword(s):  
Serum Creatinine ◽  
Protective Effect ◽  
Renal Toxicity ◽  
Methanolic Extract ◽  
Male Rats ◽  
Milk Thistle ◽  
Tubular Damage ◽  
Cisplatin Nephrotoxicity ◽  
Tubular Necrosis ◽  
Single Intraperitoneal Injection

The protective effect of methanolic extract of milk thistle seeds and silymarin against cisplatin-induced renal toxicity in male rats after a single intraperitoneal injection of 3 mg kg−1 cisplatin were studied. Over 5 days, cisplatin-treated rats showed tubular necrosis and elevation in blood urea nitrogen (BUN) and serum creatinine (Scr). Pretreatment of animals with silymarin (50 mg kg−1) or extract (0.6 g kg−1) 2 h before cisplatin prevented the tubular damage. Rats treated with silymarin or extract 2 h after cisplatin had BUN and Scr significantly lower than those receiving cisplatin, but mild to moderate necrosis was observed. These results suggested that milk thistle may protect against cisplatin-induced renal toxicity and might serve as a novel combination agent with cisplatin to limit renal injury.

Temporal induction of clusterin in cisplatin nephrotoxicity.

1997 ◽  
Vol 8 (2) ◽  
pp. 302-305
Author(s):  
J R Silkensen ◽  
A Agarwal ◽  
K A Nath ◽  
J C Manivel ◽  
M E Rosenberg
Keyword(s):  
Serum Creatinine ◽  
Time Course ◽  
Tissue Injury ◽  
Kidney Tissue ◽  
Sprague Dawley ◽  
Outer Medulla ◽  
Creatinine Concentration ◽  
Cisplatin Nephrotoxicity ◽  
Tubular Necrosis ◽  
Outer Stripe

Clusterin is a ubiquitous glycoprotein induced in many organs, including the kidney, at times of tissue injury and/or remodeling. It is speculated in this study that clusterin preserves cell interactions that are otherwise perturbed by renal insults. The purpose of this study was to examine clusterin expression after cisplatin nephrotoxicity, a model characterized by a delayed time course of injury and a well-defined site of that injury (proximal tubule). Sprague-Dawley rats were treated with intravenous cisplatin (6 mg/kg) or vehicle. Serum creatinine concentrations were measured and kidneys harvested at 1, 2, and 5 days. Marked induction of clusterin mRNA was seen only at 5 days, a time when serum creatinine concentration was the highest. Histology of kidney tissue 5 days after cisplatin administration revealed marked tubular necrosis localized to the outer stripe of the outer medulla, a region rich in proximal tubules. Immunohistochemistry and in situ hybridization at 5 days demonstrated clusterin primarily in the inner stripe of the outer medulla. In conclusion, expression of clusterin follows renal injury with cisplatin at a time corresponding to the morphologic evidence of tubular necrosis and cell detachment; quite surprisingly, such expression occurs at a site distant from the primary injury.

scholarly journals Alleviation of doxorubicin-induced nephrotoxicity by Clerodendrum volubile leaf extract in Wistar rats: A preliminary study

2020 ◽  
Vol 9 (2) ◽  
pp. 138-144 ◽  
Author(s):  
Olorunfemi Raphael Molehin
Keyword(s):  
Leaf Extract ◽  
Renal Damage ◽  
Renal Toxicity ◽  
Methanolic Extract ◽  
Male Rats ◽  
Control Group ◽  
Antioxidant Parameters ◽  
Group A ◽  
Preliminary Study ◽  
Pre Treatment

Introduction: Doxorubicin (DOX), a well-known chemotherapeutic drug, has been reported to induce numerous toxic side effects including renal toxicity. This preliminary study was designed to investigate the ameliorative effects of methanolic leaf extract of Clerodendrum volubile (MECV) against DOX-induced nephrotoxicity in rats. Methods: Thirty male rats were divided into five groups; (a) Control group: rats were given 0.9% NaCl as vehicle, (b) DOX group: a single dose of DOX (25 mg/kg; i.p.) was administered and the rats were sacrificed 4 days after DOX injection, (c-e) Methanolic extract of C. volubile (MECV)-treated DOX groups: rats were given MECV (at the doses of 125, 250 and 500 mg/kg/d), respectively for 12 consecutive days, 8 days before and 4 days after the DOX administration. Results: DOX injection caused a significant increase (P<0.05) in serum creatinine and urea levels. The levels of renal antioxidant parameters: glutathione peroxidase, superoxide dismutase (SOD), catalase (CAT) and reduced glutathione were significantly (P<0.05) decreased in DOX-intoxicated rats with concomitant elevation of malondialdehyde level. Pretreatment with MECV restored antioxidant status, attenuated oxidative stress and improved kidney function markers. Pre-treatment with MECVprotected renal tissues against DOX-induced nephrotoxicity. Conclusion: The ameliorative effects of C. volubile leaves on these renal biochemical parameters may be via its antioxidant action and may serve as a novel combination agent with DOX to limit its renal damage.

scholarly journals Protective effect of curcumin on busulfan-induced renal toxicity in male rats

Renal Failure ◽  
2020 ◽  
Vol 42 (1) ◽  
pp. 969-977
Author(s):  
Mohammad-Amin Abdollahifar ◽  
Vahid Ebrahimi ◽  
Abbas Aliaghaei ◽  
Amir Raoofi ◽  
Amirreza Khosravi ◽  
...  
Keyword(s):  
Protective Effect ◽  
Renal Toxicity ◽  
Male Rats

scholarly journals Influence of Sevoflurane on the Metabolism and Renal Effects of Compound A in Rats

2005 ◽  
Vol 103 (6) ◽  
pp. 1183-1188 ◽  
Author(s):  
Evan D. Kharasch ◽  
Jesara L. Schroeder ◽  
Pam Sheffels ◽  
H Denny Liggitt
Keyword(s):  
Serum Creatinine ◽  
Renal Toxicity ◽  
Urine Volume ◽  
Male Rats ◽  
Sevoflurane Anesthesia ◽  
Urea Nitrogen ◽  
Compound A ◽  
Renal Effects ◽  
Protein Excretion

Background The sevoflurane degradation product compound A is nephrotoxic in rats. In contrast, patient exposure to compound A during sevoflurane anesthesia has no clinically significant renal effects. The mechanism for this difference is incompletely understood. One possibility is that the metabolism and toxicity of compound A in humans is prevented by sevoflurane. However, the effect of sevoflurane on compound A metabolism and nephrotoxicity is unknown. Thus, the purpose of this investigation was to determine the effect of sevoflurane on the metabolism and renal toxicity of compound A in rats. Methods Male rats received 0.25 mmol/kg intraperitoneal compound A, alone and during sevoflurane anesthesia (3%, 1.3 minimum alveolar concentration, for 3 h). Compound A metabolites in urine were quantified, and renal function was evaluated by serum creatinine and urea nitrogen, urine volume, osmolality, protein excretion, and renal tubular histology. Results Sevoflurane coadministration with compound A inhibited compound A defluorination while increasing relative metabolism through pathways of sulfoxidation and beta-lyase-catalyzed metabolism, which mediate toxicity. Sevoflurane coadministration with compound A increased some (serum creatinine and urea nitrogen, and necrosis) but not other (urine volume, osmolality, and protein excretion) indices of renal toxicity. Conclusions Sevoflurane does not suppress compound A nephrotoxicity in rats in vivo. These results do not suggest that lack of nephrotoxicity in surgical patients exposed to compound A during sevoflurane anesthesia results from an inhibitory effect of sevoflurane on compound A metabolism and toxicity. Rather, these results are consistent with differences between rats and humans in compound A exposure and inherent susceptibility to compound A nephrotoxicity.

scholarly journals Protective effect of dapagliflozin on colistin-induced renal toxicity

2021 ◽  
Keyword(s):  
Protective Effect ◽  
Cell Injury ◽  
Saline Solution ◽  
Renal Toxicity ◽  
Multiple Drug Resistance ◽  
Tubular Epithelial Cell ◽  
Male Rats ◽  
Control Group ◽  
Multiple Drug ◽  
Group B

Objectives: Multiple-drug resistance to Gram-negative bacteria has increased signifi-cantly in recent years. Colistin is increasingly used as a last line of defense against these bacteria. However, colistin has been associated with nephrotoxicity in experimental animals. This study explores the protective effect of dapagliflozin in a rodent model of nephrotoxicity. Material Method: The present study includes a total of 24 male rats, of which 16 were given a single 20 mg/kg dose of colistin (Colimycin 150 mg/mL) intravenously to induce renal toxicity. The remaining eight rats were given no drugs in order to serve as the control, Group A. The 16 rats treated with colistin were then divided into two groups. Rats in Group B received 0.9% NaCl saline solution at a dose of 30 mL/kg/day intraperitoneally (i.p.) and 10 mg/kg/day dapagliflozin (Forziga 10 mg) via oral gavage. Those in Group C received 0.9% NaCl saline solution at an i.p. dose of 30 mL/kg/day. Both saline and dapagliflozin were administered as described over the course of ten days. The animals were euthanized and blood samples were taken by cardiac puncture for further analysis. Their kidneys were removed for histopathological and biochemical examination. Results: Levels of creatinine, BUN, KIM-1, and MDA were significantly increased in the 16-rat (Groups B and C) treatment group, in comparison to the control group; however, these biomarkers were significantly normalized in Group B, which had received dapagliflozin in addition to saline. The GSH levels of Group C showed significant decline when compared to those of the control group, and were significantly normalized in Group B. Histologically, in Group 2, we observed severe tubular dilatation and tubular epithelial cell injury in comparison to the control group. These severe anatomical changes were decreased in Group B. Conclusion: Apart from its positive effect on glucose regulation, which is the usual purpose of dapagliflozin, we observed that in colistin-induced nephrotoxicity, it decreases oxidative stress by inhibiting SGLT-2, and has restorative effects in terms of histopathology and biochemistry. These findings offer hope that the use of dapagliflozin may be protective for contrast nephropathy, which causes renal tubule damage through oxidative mechanisms. Future studies will further clarify the mechanistic action of colistin and dapagliflozin, and may support the hypothesis that dapagliflozin can be used as an adjunctive therapy in all nephrotoxic conditions.

scholarly journals The Protective Effect of Carvacrol on Acetaminophen-Induced Renal Damage in Male Rats

2021 ◽  
Author(s):  
Alireza Najafizadeh ◽  
Ayat Kaeidi ◽  
Mohammadreza Rahmani ◽  
Elham Hakimizadeh ◽  
jalal Hassanshahi
Keyword(s):  
Oxidative Stress ◽  
Serum Creatinine ◽  
Protective Effect ◽  
Renal Damage ◽  
Caspase 3 ◽  
Kidney Tissue ◽  
Group Versus ◽  
Expression Level ◽  
Male Rats ◽  
Sod Activity

Abstract Acetaminophen overdose causes renal injury via oxidative stress and apoptosis induction. Carvacrol has antioxidant effect. The aim of this study was to determine the protective effect of carvacrol on acetaminophen-induced renal damage in male rats. In this experimental study, forty male Wistar rats were randomly divided to five groups (n = 8) including control, carvacrol 10 mg/kg, acetaminophen, acetaminophen + carvacrol 5 mg/kg, and acetaminophen + carvacrol 10 mg/kg. Animals initially received a single dose of acetaminophen (500 mg/kg), then were treated with carvacrol for one week (daily). Afterwards, renal blood flow (RBF), mean arterial pressure (MAP), renal perfusion pressure (RPP), renal vascular resistance (RVR), blood urea nitrogen (BUN), and serum creatinine were measured. Also, malondialdehyde (MDA) concentration, glutathione peroxidase (GPx) and superoxide dismutase (SOD) activity levels were measured in the kidney tissue. Hematoxylin and eosin method was used for histological assessment. The western blotting analysis was used to determine the Bax, Bcl-2 and cleaved caspase-3 proteins expression level in the kidney tissue. Carvacrol (10 mg/kg) could significantly increase the RBF, GPx and SOD activities and also reduced the RVR, serum creatinine, BUN, and MDA in the acetaminophen + carvacrol 10 mg/kg group versus acetaminophen group (P < 0.05). Also, carvacrol significantly decreased the cleaved caspase-3, Bax proteins expression level, and also kidney tissue damage score in the acetaminophen + carvacrol 10 mg/kg group versus acetaminophen group (P < 0.05). This study showed that carvacrol can attenuate the acetaminophen induced acute kidney damage via suppressing oxidative stress, apoptosis and its antioxidant effects.

Protective effect of N-acetylcysteine on experimental chronic cadmium nephrotoxicity in immature female rats

2009 ◽  
Vol 28 (4) ◽  
pp. 221-229 ◽  
Author(s):  
L Wang ◽  
D Chen ◽  
J Cao ◽  
Z Liu
Keyword(s):  
Protective Effect ◽  
Antioxidant Properties ◽  
Female Rats ◽  
Tubular Damage ◽  
Sprague Dawley ◽  
Tubular Necrosis ◽  
Sprague Dawley Rats ◽  
Nonenzymatic Antioxidants ◽  
Renal Tubular ◽  
Enzyme Markers

In the present study, female Sprague-Dawley rats received CdCl2 (50 mg/L through drinking water) and/or N-acetylcysteine (NAC, 120 mg/kg/day, orally) to investigate the protective effect of NAC on Cd-induced renal damage. Renal toxicity was evaluated by measuring the contents of total protein, β2-microglobulin, and α1-microglobulin in the urine and urinary enzyme markers of tubular necrosis, as well as levels of serum urea nitrogen and serum creatinine. Activities of antioxidant enzymes and contents of glutathione, malondialdehyde, and trace elements in the kidney were also measured. Animals that received both Cd and NAC showed a better renal function than those receiving Cd alone. In addition, NAC significantly reduced the levels of lipid peroxidation (LPO) in the kidney of cadmium-treated rats. The enzymic and nonenzymatic antioxidants levels are not restored, but their further decrease is prevented by NAC. Also NAC administration does not modify the urinary excretion of cadmium or contents of cadmium in the serum and kidney. In conclusion, NAC exerts its protective effect by decreased LPO and improving antioxidants status to prevent renal tubular damage induced by chronic Cd administration, most probably through its antioxidant properties.

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