Coenzyme Q10 Attenuates Cisplatin-induced Nephrotoxicity Through Counteracting Oxidative Stress and Inflammation

2019 ◽  
Vol 6 (1) ◽  
pp. 41-47
Author(s):  
Hala S. Bash ◽  
Ihsan S. Rabeea
Keyword(s):  
Oxidative Stress ◽  
Serum Creatinine ◽  
Coenzyme Q10 ◽  
Kidney Injury ◽  
Treated Group ◽  
Control Group ◽  
Histopathological Analysis ◽  
Adult Rats ◽  
Necrosis Factor Alpha ◽  
Kidney Injury Molecule 1

Background: Cisplatin is an anticancer drug used in the management of solid tumors, however, dose-related nephrotoxicity is one of its major problems. Agents having antioxidants, antiinflammatory and/or antiapoptotic activities may thus represent potential therapeutic options to avoid cisplatin-induced nephrotoxicity. Among these agents, coenzyme Q10 has several pharmacological properties including antioxidant, anti-inflammatory and/or anti-apoptotic effects. Objective: The current study aimed to examine whether coenzyme Q10 could attenuate cisplatininduced nephrotoxicity or not. Methods: 24 adult rats were randomly separated into three groups (8 rats per group). The first one was the control group, rats receiving vehicle (olive oil) intraperitoneally. The second group was Cisplatin treated group, rats were receiving 13 mg/kg of Cisplatin intraperitoneally as a single dose. The third group (Cisplatin + Coenzyme Q10), rats were receiving 13 mg/kg as a single intraperitoneal dose of Cisplatin and coenzyme Q10 daily for six consecutive days (10 mg/kg intraperitoneally). Results: Cisplatin caused significant increases in serum creatinine and severe histological lesions. Cisplatin treated group also showed a significant elevation in renal malondialdehyde concentration as a marker of oxidative stress; renal tumor necrosis factor-alpha concentration as a marker of inflammation; and Kidney injury molecule -1 concentration. Coenzyme Q10 significantly attenuated cisplatininduced nephrotoxicity through lowering serum creatinine and improving nephrotoxicity histological scores. Coenzyme Q10 also significantly reduced the renal concentration of MDA, TNF-α and KIM-1 relative to cisplatin treated group. Conclusions: Coenzyme Q10 has a potential nephroprotective effect against cisplatin-induced nephrotoxicity that was demonstrated by biochemical and histopathological analysis.

scholarly journals D-Limonene Alleviates Acute Kidney Injury Following Gentamicin Administration in Rats: Role of NF-κB Pathway, Mitochondrial Apoptosis, Oxidative Stress, and PCNA

2021 ◽  
Vol 2021 ◽  
pp. 1-16
Author(s):  
Esmaeel Babaeenezhad ◽  
Forouzan Hadipour Moradi ◽  
Sobhan Rahimi Monfared ◽  
Mohammad Davood Fattahi ◽  
Maryam Nasri ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Acute Kidney Injury ◽  
Kidney Injury ◽  
Treated Group ◽  
Control Group ◽  
Myeloperoxidase Activity ◽  
Protective Effects ◽  
Mitochondrial Apoptosis ◽  
Protein Expressions ◽  
Apoptosis And Inflammation

Clinical application of gentamicin (GM) is well known to be associated with the development of acute kidney injury (AKI). This study was the first to investigate the possible protective effects of D-limonene (D-lim) on AKI following GM administration in rats. 32 rats arranged in four groups ( n = 8 ): (1) the control group received saline intraperitoneally (0.5 ml/day) and orally (0.5 ml/day), (2) the D-lim group received D-lim (100 mg/kg) orally and saline (0.5 ml/day) intraperitoneally, (3) the GM group received GM (100 mg/kg/day) intraperitoneally and saline (0.5 ml/day) orally, and (4) the treated group received intraperitoneal GM (100 mg/kg) and oral D-lim (100 mg/kg). All treatments were performed daily for 12 consecutive days. Results revealed that D-lim ameliorated GM-induced AKI, oxidative stress, mitochondrial apoptosis, and inflammation. D-lim showed nephroprotective effects as reflected by the decrease in serum urea and creatinine and improvement of renal histopathological changes. D-lim alleviated GM-induced oxidative stress by increasing the activities of renal catalase, serum and renal glutathione peroxidase, and renal superoxide dismutase and decreasing renal malondialdehyde and serum nitric oxide levels. Intriguingly, D-lim suppressed mitochondrial apoptosis by considerably downregulating Bax and caspase-3 (Casp-3) mRNA and protein expressions and markedly enhancing Bcl2 mRNA and protein expressions. Furthermore, D-lim significantly decreases GM-induced inflammatory response through downregulation of NF-κB, IL-6, and TNF-α mRNA and/or protein expressions and decrease in renal myeloperoxidase activity. Finally, D-lim remarkably downregulated PCNA protein expression in the treated group compared with the GM group. In brief, this study showed that D-lim alleviated AKI following GM administration in rats, partially through its antioxidant, anti-inflammatory, and antiapoptotic activities as well as downregulation of PCNA expression.

Evaluation the effect of Ginkgo Biloba and Coenzyme Q10 on Doxorubicin-induced acute cardiotoxicity in rats

2018 ◽  
Vol 9 (SPL1) ◽  
Author(s):  
Samer Tariq Jasim
Keyword(s):  
Single Dose ◽  
Serum Level ◽  
Drug Administration ◽  
Coenzyme Q10 ◽  
Ginkgo Biloba ◽  
Normal Saline ◽  
Treated Group ◽  
Control Group ◽  
Necrosis Factor Alpha ◽  
Acute Cardiotoxicity

Doxorubicin,an anthracycline antibiotic is a powerful antineoplastic drug,but its therapeutic usefulness is limited by its cardiotoxicity. The present study investigated the influence of pretreatment with Ginkgo biloba and Coenzyme Q10 alone or in combination on doxorubicin induced acute cardiotoxicity in rats regarding biochemical and histological approaches. 30 rats were divided randomly into five groups each contain six rats. The first group received normal saline (5ml/kg,ip) daily for ten days,which considered as control group. The second group received normal saline (5ml/kg,ip) daily for ten days and then doxorubicin single dose (20mg/kg,ip) on 8th day,which considered as doxorubicin group. The third group treated with Ginkgo Biloba (100mg/kg,po) daily for ten successive days,and on 8th day,one hour after drug administration,doxorubicin single dose (20mg/kg,ip) was given. The fourth group treated with Coenzyme Q10 (50mg/kg,po),daily for ten successive days,and on 8th day,doxorubicin single dose (20mg/kg,ip) was given. The fifth group treated with both Ginkgo Biloba (100mg/kg,po) and Coenzyme Q10 (50mg/kg,po), daily for ten successive days,and on 8th day,one hour after drug administration,doxorubicin single dose (20mg/kg,ip) was given. At 11th day of the study,blood samples were taken for biochemical analysis,then animals were sacrificed and hearts were taken for histopathological observations. Rats treated with doxorubicin showed cardiotoxicity as evidenced by significant elevation of serum cardiac troponin (cTn-I) level,serum malondialdehyde (MDA) level,brain natriuretic peptide (BNP) serum level,Caspase-3 serum level, (LPO) serum level,and Tumor necrosis factor alpha (TNF-α),and significant reduction in glutathione peroxide serum level associated with important histopathological alterationswhile pre-treatment with Ginkgo biloba and Coenzyme Q10 elicited a significant decrease in the activities of all markers measured in comparison with doxorubicin treated group with pronounced resolution of doxoribicin-induced cardiac histopathological changes to a milder picture. These results suggest pretreatment with Ginkgo biloba and Coenzyme Q10 alone or in combination provide a significant protective effect against acute-doxorubicin induced cardiotoxicity in rats represented by biochemical markers and histological approaches.

scholarly journals The Nephroprotective Effect of Zizyphus lotus L. (Desf.) Fruits in a Gentamicin-Induced Acute Kidney Injury Model in Rats: A Biochemical and Histopathological Investigation

Molecules ◽  
2021 ◽  
Vol 26 (16) ◽  
pp. 4806
Author(s):  
Noureddine Bencheikh ◽  
Mohamed Bouhrim ◽  
Loubna Kharchoufa ◽  
Omkulthom Mohamed Al Kamaly ◽  
Hamza Mechchate ◽  
...  
Keyword(s):  
Uric Acid ◽  
Kidney Injury ◽  
Treated Group ◽  
Renal Tissue ◽  
Control Group ◽  
Histopathological Analysis ◽  
Distilled Water ◽  
Gamma Glutamyl Transpeptidase ◽  
Injury Model ◽  
Biochemical Observation

Zizyphus lotus L. (Desf.) (Z. lotus) is a medicinal plant largely distributed all over the Mediterranean basin and is traditionally used by Moroccan people to treat many illnesses, including kidney failure. The nephrotoxicity of gentamicin (GM) has been well documented in humans and animals, although the preventive strategies against it remain to be studied. In this investigation, we explore whether the extract of Zizyphus lotus L. (Desf.) Fruit (ZLF) exhibits a protective effect against renal damage produced by GM. Indeed, twenty-four Wistar rats were separated into four equal groups of six each (♂/♀ = 1). The control group was treated orally with distilled water (10 mL/kg); the GM treated group received distilled water (10 mL/kg) and an intraperitoneal injection of GM (80 mg/kg) 3 h after; and the treated groups received ZLF extract orally at the doses 200 or 400 mg/kg and injected intraperitoneally with the GM. All treatments were given daily for 14 days. At the end of the experiment, the biochemical parameters and the histological observation related the kidney function was explored. ZLF treatment has significantly attenuated the nephrotoxicity induced by the GM. This effect was indicated by its capacity to decrease significantly the serum creatinine, uric acid, urea, alkaline phosphatase, gamma-glutamyl-transpeptidase, albumin, calcium, sodium amounts, water intake, urinary volume, and relative kidney weight. In addition, this effect was also shown by the increase in the creatinine clearance, urinary creatinine, uric acid, and urea levels, weight gain, compared to the rats treated only with the GM. The hemostasis of oxidants/antioxidants has been significantly improved with the treatment of ZLF extract, which was shown by a significant reduction in malondialdehydes levels. Histopathological analysis of renal tissue was correlated with biochemical observation. Chemical analysis by HPLC-DAD showed that the aqueous extract of ZLF is rich in phenolic compounds such as 3-hydroxycinnamic acid, catechin, ferulic acid, gallic acid, hydroxytyrosol, naringenin, p- coumaric Acid, quercetin, rutin, and vanillic acid. In conclusion, ZLF extract improved the nephrotoxicity induced by GM, through the improvement of the biochemical and histological parameters and thus validates its ethnomedicinal use.

scholarly journals Mitigation of cisplatin induced nephrotoxicity by casticin in male albino rats

2023 ◽  
Vol 83 ◽  
Author(s):  
N. Ehsan ◽  
M. U. Ijaz ◽  
A. Ashraf ◽  
S. Sarwar ◽  
A. Samad ◽  
...  
Keyword(s):  
Kidney Injury ◽  
Thiobarbituric Acid ◽  
Treated Group ◽  
Free Radical Scavenger ◽  
Control Group ◽  
Albino Rats ◽  
Radical Scavenger ◽  
Neutrophil Gelatinase Associated Lipocalin ◽  
Group 2 ◽  
Kidney Injury Molecule 1

Abstract Cisplatin (CP) is a commonly used, powerful antineoplastic drug, having numerous side effects. Casticin (CAS) is considered as a free radical scavenger and a potent antioxidant. The present research was planned to assess the curative potential of CAS on CP persuaded renal injury in male albino rats. Twenty four male albino rats were distributed into four equal groups. Group-1 was considered as a control group. Animals of Group-2 were injected with 5mg/kg of CP intraperitoneally. Group-3 was co-treated with CAS (50mg/kg) orally and injection of CP (5mg/kg). Group-4 was treated with CAS (50mg/kg) orally throughout the experiment. CP administration substantially reduced the activities of catalase (CAT), superoxide dismutase (SOD), peroxidase (POD), glutathione S-transferase (GST), glutathione reductase (GSR), glutathione (GSH) content while increased thiobarbituric acid reactive substances (TBARS), and hydrogen peroxide (H2O2) levels. Urea, urinary creatinine, urobilinogen, urinary proteins, kidney injury molecule-1 (KIM-1), and neutrophil gelatinase-associated lipocalin (NGAL) levels were substantially increased. In contrast, albumin and creatinine clearance was significantly reduced in CP treated group. The results demonstrated that CP significantly increased the inflammation indicators including nuclear factor kappa-B (NF-κB), tumor necrosis factor-α (TNF-α), Interleukin-1β (IL-1β), Interleukin-6 (IL-6) levels and cyclooxygenase-2 (COX-2) activity and histopathological damages. However, the administration of CAS displayed a palliative effect against CP-generated renal toxicity and recovered all parameters by bringing them to a normal level. These results revealed that the CAS is an effective compound having the curative potential to counter the CP-induced renal damage.

scholarly journals Cinnabar Induces Renal Inflammation and Fibrogenesis in Rats

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Ying Wang ◽  
Dapeng Wang ◽  
Jie Wu ◽  
Bohan Wang ◽  
Liangjun Wang ◽  
...  
Keyword(s):  
Serum Creatinine ◽  
Kidney Injury ◽  
Inflammatory Cells ◽  
Control Group ◽  
Mesangial Proliferation ◽  
Renal Inflammation ◽  
Urinary Mercury ◽  
Time Periods ◽  
Kidney Injury Molecule 1 ◽  
Kidney Lesions

The purpose of this study was to investigate whether cinnabar causes renal inflammation and fibrosis in rats. Rats were dosed orally with cinnabar (1 g/kg/day) for 8 weeks or 12 weeks. The control rats were treated with solvent (5% carboxymethylcellulose solution) over the same time periods, respectively. Renal mercury (RHg), urinary mercury (UHg), serum creatinine (SCr), urine kidney injury molecule 1 (KIM-1), renal pathology, and renal mediators were examined. At both 8 weeks and 12 weeks, RHg, UHg, and urine KIM-1 were significantly higher in the cinnabar group than in the control group, although SCr was unchanged. Kidney lesions in the cinnabar-treated rats occurred mainly in the tubules and interstitium, including vacuolization, protein casts, infiltration of inflammatory cells, and slight increase in interstitial collagen. In addition, mild mesangial proliferation was observed in glomeruli. Moreover, the expression of inflammatory and fibrogenic mediators was upregulated in the cinnabar group. In conclusion, cinnabar may cause kidney damage due to the accumulation of mercury, and renal inflammation and slight fibrogenesis may occur in rats. In the clinic, the potential risk of renal injury due to the prolonged consumption of cinnabar should be considered even though the agent is relatively nontoxic.

scholarly journals Protective Effect of Astaxanthin on Ochratoxin A-Induced Kidney Injury to Mice by Regulating Oxidative Stress-Related NRF2/KEAP1 Pathway

Molecules ◽  
2020 ◽  
Vol 25 (6) ◽  
pp. 1386 ◽  
Author(s):  
Lin Li ◽  
Yueli Chen ◽  
Danyang Jiao ◽  
Shuhua Yang ◽  
Lin Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzymes ◽  
Epithelial Cells ◽  
Ochratoxin A ◽  
Kidney Injury ◽  
Treated Group ◽  
Serum Markers ◽  
Control Group ◽  
Heme Oxygenase 1 ◽  
Ultrastructural Observation

The present study aimed to investigate the effects of astaxanthin (ASX) on ochratoxin A (OTA)-induced renal oxidative stress and its mechanism of action. Serum kidney markers, histomorphology, ultrastructural observation, and oxidative stress indicators were assessed. Meanwhile, quantitative real-time reverse transcription PCR and western blotting detection of NRF2 (encoding nuclear factor, erythroid 2 like) and members of the NRF2/KEAP1 signaling pathway (KEAP1 (encoding Kelch-like ECH-associated protein), NQO1 (encoding NAD(P)H quinone dehydrogenase), HO-1 (encoding heme oxygenase 1), γ-GCS (gamma-glutamylcysteine synthetase), and GSH-Px (glutathione peroxidase 1)) were performed. Compared with the control group, the OTA-treated group showed significantly increased levels of serum UA (uric acid) and BUN (blood urea nitrogen), tubular epithelial cells were swollen and degenerated, and the levels of antioxidant enzymes decreased significantly, and the expression of NRF2 (cytoplasm), NQO1, HO-1, γ-GCS, and GSH-Px decreased significantly. More importantly, after ASX pretreatment, compared with the OTA group, serum markers were decreased, epithelial cells appeared normal; the expression of antioxidant enzymes increased significantly, NQO1, HO-1, γ-GCS and GSH-Px levels increased significantly, and ASX promoted the transfer of NRF2 from the cytoplasm to the nucleus. These results highlight the protective ability of ASX in renal injury caused by OTA exposure, and provide theoretical support for ASX’s role in other mycotoxin-induced damage.

Alleviation of doxorubicin–induced hepatorenal toxicities with sesamin via the suppression of oxidative stress

2016 ◽  
Vol 35 (11) ◽  
pp. 1183-1193 ◽  
Author(s):  
H Guo ◽  
Y Liu ◽  
L Wang ◽  
G Zhang ◽  
S Su ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Activity ◽  
Alkaline Phosphatase ◽  
Serum Creatinine ◽  
Kidney Injury ◽  
Treated Group ◽  
Anthracycline Antibiotics ◽  
Histological Damage ◽  
Liver And Kidney ◽  
Mda Content

Hepatorenal toxicities are an important side effect of anthracycline antibiotics. The objective of this study was to determine whether sesamin (Ses) protects against acute doxorubicin (DOX)-induced hepatorenal toxicities. Rats received daily treatment with either 0.5% carboxymethylcellulose (10 mL/kg) or Ses (10, 20 and 40 mg/kg) orally for 10 days, followed by an intravenous injection at day 8 of either saline (10 mL/kg) or DOX (20 mg/kg). Hepatorenal toxicity was assessed by measuring the levels of serum creatinine (Cre), blood urea nitrogen (BUN), aspartate aminotransferase (AST), alanine aminotransferase (ALT) and alkaline phosphatase (ALP). The protein expression of 4-hydroxynonenal (4-HNE) in hepatorenal tissues was evaluated using immunohistochemistry. The malondialdehyde (MDA) content and antioxidant activity in the kidney and liver tissues were also measured. The results suggest that pretreatment with Ses ameliorated DOX-induced liver and kidney injury by lowering the serum ALT, AST, ALP, Cre and BUN levels ( p < 0.05 or p < 0.01), and the histological damage to the liver and kidney tissues induced by DOX compared to control were also significantly attenuated by Ses. Furthermore, Ses significantly decreased the DOX-induced increase of MDA and 4-HNE and increased the activity of CAT, SOD and GPX compared to the DOX-treated rats ( p < 0.05 or p < 0.01), whereas the change of DOX + Ses (10 mg/kg) group is not significant compared to the DOX-treated group ( p > 0.05). These findings indicate that Ses elicits a typical protective effect against DOX-induced acute hepatorenal toxicity via the suppression of oxidative stress.

scholarly journals Cinnabar-Induced Subchronic Renal Injury Is Associated with Increased Apoptosis in Rats

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Ying Wang ◽  
Dapeng Wang ◽  
Jie Wu ◽  
Bohan Wang ◽  
Xianhui Gao ◽  
...  
Keyword(s):  
Renal Injury ◽  
Death Receptor ◽  
Kidney Injury ◽  
Inflammatory Cells ◽  
Underlying Mechanism ◽  
Treated Group ◽  
Control Group ◽  
Antibody Array ◽  
Tubular Cells ◽  
Kidney Injury Molecule 1

The aim of this study was to explore the role of apoptosis in cinnabar-induced renal injury in rats. To test this role, rats were dosed orally with cinnabar (1 g/kg/day) for 8 weeks or 12 weeks, and the control rats were treated with 5% carboxymethylcellulose solution. Levels of urinary mercury (UHg), renal mercury (RHg), serum creatinine (SCr), and urine kidney injury molecule 1 (KIM-1) were assessed, and renal pathology was analyzed. Apoptotic cells were identified and the apoptotic index was calculated. A rat antibody array was used to analyze expression of cytokines associated with apoptosis. Results from these analyses showed that UHg, RHg, and urine KIM-1, but not SCr, levels were significantly increased in cinnabar-treated rats. Renal pathological changes in cinnabar-treated rats included vacuolization of tubular cells, formation of protein casts, infiltration of inflammatory cells, and increase in the number of apoptotic tubular cells. In comparison to the control group, expression of FasL, Fas, TNF-α, TRAIL, activin A, and adiponectin was upregulated in the cinnabar-treated group. Collectively, our results suggest that prolonged use of cinnabar results in kidney damage due to accumulation of mercury and that the underlying mechanism involves apoptosis of tubular cells via a death receptor-mediated pathway.

scholarly journals 6-Gingerol, a Major Ingredient of Ginger Attenuates Diethylnitrosamine-Induced Liver Injury in Rats through the Modulation of Oxidative Stress and Anti-Inflammatory Activity

2021 ◽  
Vol 2021 ◽  
pp. 1-17
Author(s):  
Mohammed A. Alsahli ◽  
Saleh A. Almatroodi ◽  
Ahmad Almatroudi ◽  
Amjad Ali Khan ◽  
Shehwaz Anwar ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Function ◽  
Inflammatory Markers ◽  
Liver Diseases ◽  
Treated Group ◽  
Control Group ◽  
Histopathological Analysis ◽  
Tnf Α ◽  
Hepatoprotective Effects ◽  
Anti Inflammatory

Diethylnitrosamine (DEN) is a well-known hepatocarcinogen, and its oral administration causes severe liver damage including cancer. DEN induces the pathogenesis of the liver through reactive oxygen species mediated inflammation and modulation of various biological activities. 6-Gingerol, a major component of ginger, is reported to prevent liver diseases by reducing the oxidative stress and proinflammatory mediators. The present study investigated the hepatoprotective effects of 6-gingerol through the measurement of oxidative stress, anti-inflammatory markers, liver function enzyme parameter, and histopathological analysis. The rats were randomly divided into four groups as the control, DEN treated (50 mg/kg b.w.), DEN+6-gingerol (each 50 mg/kg b.w.), and 6-gingerol only. To evaluate the hepatoprotective effects, liver function enzymes (ALT, AST, and ALP), oxidative stress markers (SOD, GSH, GST, and TAC), lipid peroxidation, inflammatory markers (CRP, TNF-α, IL-6, and ICAM1), haematoxylin and eosin staining, Sirius red staining, immunohistochemistry, and electron microscopy were performed. The results showed a significant increase in liver function enzymes, oxidative stress, and inflammatory markers in the DEN-treated group as compared to the control group. Besides this, altered architecture of hepatocytes (infiltration of inflammatory cells, congestion, blood vessel dilation, and edema), abundant collagen fiber and organelle structures like distorted shaped and swollen mitochondria, and broken endoplasmic reticulum were noticed. The administration of 6-gingerol significantly ameliorated the biochemical and histopathological changes. The increased expression of TNF-α protein was noticed in the DEN-treated group whereas the administration of 6-gingerol significantly decreased the expression of this protein. Based on these findings, it can be suggested that 6-gingerol may be an alternative therapy for the prevention and treatment of liver diseases.

scholarly journals Pioglitazone attenuates kidney injury in an experimental model of gentamicin-induced nephrotoxicity in rats

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Branislava Medić ◽  
Marko Stojanović ◽  
Branislav Rovčanin ◽  
Dušan Kekić ◽  
Sanja Radojević Škodrić ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Experimental Model ◽  
Rat Kidney ◽  
Kidney Injury ◽  
Stress Index ◽  
Control Group ◽  
Peroxisome Proliferator ◽  
Serum Urea ◽  
Pparγ Agonist ◽  
Kidney Injury Molecule 1

Abstract Gentamicin, belonging to the aminoglycosides, possesses the greatest nephrotoxic effect of all other antibiotics from this group. On the other hand, pioglitazone, which represents peroxisome proliferator-activated receptor γ (PPARγ) agonist recently showed antiinflamatory, antioxidative effects, amelioration of endothelial dysfunction etc. Therefore, the goal of our study was to investigate the effects of pioglitazone on kidney injury in an experimental model of gentamicin-induced nephrotoxicity in rats. These effects were observed by following values of biochemical (serum urea and creatinine) parametars, total histological kidney score, urine level of kidney injury molecule-1 (KIM-1) and neutrophil gelatinase-associated lipocalin (NGAL) as well as parametars of oxidative stress (malondialdehyde, superoxide dismutase, catalase, total oxidant status, total antioxidant status, oxidative stress index and advanced oxidation protein products). It seems that pioglitazone protects the injured rat kidney in a U-shaped manner. Medium dose of pioglitazone (1 mg/kg, i.p.) was protective regarding biochemical (serum urea and creatinine), total histological score and the values of kidney injury molecule-1 (KIM-1) (P < 0.05 vs. control group, i.e. rats injected with gentamicin only). This finding could be of great importance for the wider use of aminoglycosides, with therapy that would reduce the occurrence of serious adverse effects, such as nephrotoxicity and acute renal failure.

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