Protective effects of gallic acid against methotrexate-induced toxicity in rats

Background: Methotrexate, as a chemotherapy drug, can cause chronic liver damage and oxidative stress. Aim of this study was to evaluate the preventive effect of gallic acid (GA) on methotrexate (MTX)-induced oxidative stress in rat liver.

Methods: Twenty-eight male rats were randomly divided into four groups as control, MTX (20?mg/kg, i.p.), MTX?+?GA (30?mg/kg/day, orally) and GA treated. Aspartate aminotransferase (AST), alanine aminotransferase (ALT) and alkaline phosphatase (ALP) were used as biochemical markers of MTX-induced hepatic injury. Malondialdehyde (MDA) and glutathione (GSH) levels and hepatic antioxidant enzymes activities including catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GPx) were assayed in liver tissue. The expression of SOD2 and GPx1 genes were evaluated by real-time RT-PCR and liver histopathology was evaluated by light microscopy.

Results: The result obtained from current study showed that GA remarkably reduced MTX-induced elevation of AST, ALT and ALP and increased MTX-induced reduction in GSH content, GPx, CAT and SOD activity as well as GPx1 and SOD2 gene expressions. Histological results showed that MTX led to liver damage and GA could improve histological changes.

Conclusions: Our results indicate that GA ameliorates biochemical and oxidative stress parameters in the liver of rats exposed to MTX.     

Rutin attenuates gentamicin-induced renal damage by reducing oxidative stress,inflammation, apoptosis,and autophagy in rats

Abstract

Gentamicin is commonly used against gram-negative microorganisms. Its therapeutic use is mainly limited by nephrotoxicity. This study was aimed at evaluating the effect of rutin on oxidative stress, inflammation, apoptosis, and autophagy in gentamicin-induced nephrotoxicity in rats. The rats were treated with saline intraperitoneally (group I), 150?mg/kg of rutin orally (group II), 80?mg/kg of gentamicin intraperitoneally for 8?d (group III), or 150?mg/kg of rutin plus 80?mg/kg of gentamicin (group IV). The serum urea, creatinine, kidney malondialdehyde (MDA), and reduced glutathione (GSH) levels and superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activity and protein concentration were measured, and renal histopathology analysis and immunohistochemical staining were performed. Rutin pretreatment attenuated nephrotoxicity induced by gentamicin by reducing the urea, creatinine, and MDA levels and increasing the SOD, CAT, and GPx activity, and the GSH levels. The rutin also inhibited inducible nitric oxide synthase (iNOS), cleaved caspase-3 and light chain 3B (LC3B), as evidenced by immunohistochemical staining. The present study demonstrates that rutin exhibits antioxidant, anti-inflammatory, anti-apoptotic, and anti-autophagic effects and that it attenuates gentamicin-induced nephrotoxicity in rats.     

Evaluation of the protective effect of agmatine against cisplatin nephrotoxicity with 99mTc-DMSA renal scintigraphy and cystatin-C

Background: The aim of the current study was to investigate whether agmatine (AGM) has a protective effect against cisplatin-induced nephrotoxicity.

Materials and methods: Thirty-two rats were randomly divided into four groups: (1) Saline (control); (2) Cisplatin (CDDP; 7.5?mg/kg intraperitoneally); (3) Agmatine (AGM; 10?mg/kg intraperitoneally); (4) Cisplatin plus agmatine (CDDP?+?AGM). Agmatine was given before and two consecutive days after cisplatin injection. All the animals underwent renal scintigraphy with 99mTc-DMSA. The levels of serum creatinine, cystatin C, and blood urea nitrogen (BUN) were measured in addition to examination of the tissue samples with light microscopy. Acute renal injury was assessed with biochemical analyses, scintigraphic imaging, and histopathological evaluation.

Results: In the cisplatin group, the levels of BUN, creatinine, and cystatin C were significantly higher than that of the controls. Histopathological examination showed remarkable damage of tubular and glomerular structures. Additionally, cisplatin caused markedly decreased renal 99mTc-DMSA uptake. AGM administration improved renal functions. Serum creatinine, BUN, and cystatin C levels had a tendency to normalize and, scintigraphic and histopathological findings showed significantly less evidence of renal toxicity than those observed in animals receiving cisplatin alone.

Conclusions: Our data indicate that AGM has a protective effect against cisplatin-induced nephrotoxicity. Therefore, it may improve the therapeutic index of cisplatin. In addition, the early renal damage induced by cisplatin and protective effects of AGM against cisplatin nephrotoxicity was accurately demonstrated with 99mTc-DMSA renal scintigraphy.     

Ameliorative effect of berberine against gentamicin-induced nephrotoxicity in rats via attenuation of oxidative stress,inflammation, apoptosis and mitochondrial dysfunction

Background: Gentamicin (GM) is the commonly used antibiotics against Gram-negative infection, but the nephrotoxic potential of drug limit its clinical interest. The aim of this study was to investigate the protective effect of berberine (BER) against GM-induced nephrotoxicity and possible underlying mechanisms. Material and methods: The rats were divided into various group, namely normal, GM-control, GM?+?BER (10, 20, and 40?mg/kg). Nephrotoxicity was induced by intraperitoneal administration of GM (120?mg/kg) for 7 consecutive days. BER (10, 20, and 40?mg/kg; p.o.) was also administered for the 7 days. Various biochemical, molecular, and histological parameters were assessed in serum and kidney. Results: GM-administration significantly increased (p?<?0.001) the serum creatinine and blood urea nitrogen (BUN) as well as renal malonaldehyde (MDA), nitric oxide (NO) along with Kidney Injury Molecule-1 (KIM-1), Neutrophil gelatinase-associated lipocalin (NGAL), and nuclear factor-kappa B (NF-KB) renal mRNA expressions. In addition, GM also significantly decreased (p?<?0.001) the renal superoxide dismutase (SOD), reduced glutathione (GSH), B-cell lymphoma 2 (Bcl-2) mRNA expression, and mitochondrial enzymes (NADH dehydrogenase and cytochrome c oxidase) activities. Rats treated with BER (20 and 40?mg/kg; p.o.) significantly and dose-dependently (p?<?0.05 and p?<?0.01) restore the altered levels of antioxidant, inflammatory, apoptosis, AKI markers as well as depleted mitochondrial enzymes. Histopathological abbreviations were also ameliorated by BER administration. Conclusion: Berberine exerts renoprotective effects through its anti-oxidant, anti-inflammatory, and anti-apoptotic properties.     

Renoprotective effect of berberine via intonation on apoptosis and mitochondrial-dependent pathway in renal ischemia reperfusion-induced mutilation

Abstract

Ischemic acute renal failure is a condition that extends subsequent to sudden and momentary fall in overall or regional blood flow to the kidney. The present investigation was deliberated to scrutinize the renoprotective potential of berberine in animal model of renal ischemia reperfusion (RIR) induced dent via assessment of various biochemical and molecular biomarkers. Male Wistar rats were anesthetized and the right kidney was removed through a small flank incision. Renal ischemia reperfusion was persuaded in uni-nephrectomized rats by occlusion of left renal artery for 45?min and reperfusion for 4 weeks. After 4 weeks of treatment of berberine (10, 20, and 40?mg/kg, p.o.), hemodynamic and left ventricular function were evaluated. Induction of ischemia reperfusion resulted callous mutilation in kidney which was confirmed by alterations in oxidative stress (SOD, GSH, and MDA), membrane bound enzymes, kidney function markers (serum creatinine and BUN), and mitochondrial dysfunction. Moreover, RIR injury exhibited incredible alterations in mRNA expression of KIM-1, NGAL, Caspase-3, Bax, Bcl-2, and TNF-α levels. Conversely treatment of berberine (20 and 40?mg/kg) significantly (p?<?0.01 and p?<?0.001) restored ischemia reperfusion induced marring via intonation of biochemical and molecular biomarkers. To sum up, berberine demonstrated compelling renoprotective effect in RIR injury via caspase-mitochondria-dependent pathway.     

Tetrahydrocurcumin protects against sepsis-induced acute kidney injury via the SIRT1 pathway

Sepsis-induced acute kidney injury (AKI) continues to be associated with poor outcomes in critical care patients. Previous research has revealed that tetrahydrocurcumin (THC) exerts renoprotective effects in multiple nephritic disorders by modulating inflammation and oxidative stress. However, the effects of THC on sepsis-induced AKI and the underlying mechanisms remain unclear. In this study, a mouse model of sepsis-induced AKI, generated by cecal ligation and puncture operation, was used to investigate the protective effects of THC and the role of SIRT1. Histological manifestation and TUNEL analysis were observed to determine the severity of kidney damage. Levels of BUN, SCr, KIM-1, and UAlb/Cr were calculated to assess the renal function. Expressions of IL-1β, IL-6, and TNF-α were measured to evaluate the inflammatory response. MDA content, SOD, GSH, CAT, and GPx activities and DHE staining were analyzed to estimate the degree of oxidative stress. Protein expressions of SIRT1, Ac-p65, and Ac-foxo1 were detected to explore the underlying mechanisms. We observed that THC not only increased the survival rate, improved the kidney function and ameliorated the renal histological damage of septic mice, but also inhibited inflammatory response, prohibited oxidative stress, and prevented cell apoptosis in renal tissues in septic mice. Mechanistically, THC remarkably increased the expression of SIRT1, accompanied by decreased expressions of downstream molecules Ac-p65 and Ac-foxo1. Meanwhile, the beneficial effects of THC were clearly abolished by the SIRT1-specific inhibitor EX527. These results delineate that THC prevents sepsis-induced AKI by suppressing inflammation and oxidative stress through activating the SIRT1 signaling.Abbreviation: Ac-p65: acetylated p65; Ac-foxo 1: acetylated forkhead box O1; AKI: acute kidney injury; BUN: blood urea nitrogen; CAT: catalase; DHE: dihydroethidium; GPx: glutathione peroxidase; GSH: reduced glutathione; IL-1β: Interleukin-1 beta; IL-6: Interleukin-6; KIM-1: kidney injury molecule 1; MDA: malondialdehyde; SCr: serum creatinine; SIRT1: silent information regulator 1; SOD: superoxide dismutase; THC: tetrahydrocurcumin; TNF-α: tumor necrosis factor-alpha; TUNEL: TdT-mediated dUTP Nick-End Labeling; UAlb/Cr: urine micro albumin/creatinine.     

羟考酮预给药对大鼠肾缺血-再灌注损伤的影响

目的评价羟考酮预给药对大鼠肾缺血-再灌注损伤的影响。方法健康成年雄性SD大鼠30只,采用随机数字表法,将其分为三组(n=10),假手术组(S组):仅切除右肾、分离左侧肾动脉、肾静脉和输尿管;缺血-再灌注组(IR组):切除右侧肾脏,夹闭左侧肾动脉和肾静脉45min恢复灌注2h;羟考酮预给药+缺血-再灌注组(O组):缺血-再灌注前5min静脉注射羟考酮2mg/kg。于再灌注2h时经腹主动脉采集动脉血样,血清尿素氮(BUN)浓度采用脲酶法测定,血清肌酐(Cr)浓度采用速率法测定。处死大鼠,取部分左肾组织,超氧化物歧化酶(SOD)活性采用黄嘌呤氧化酶法测定,丙二醛(MDA)含量采用硫代巴比妥酸法测定。采用Western blot检测肾组织中B细胞淋巴瘤/白血病-2(bcl-2)、B细胞淋巴瘤/白血病-2相关x蛋白(bax)、半胱氨酸天冬氨酸蛋白酶-3(Caspase-3)蛋白表达。结果与S组比较,IR组和O组血清BUN和Cr的浓度明显升高(P0.05),肾组织MDA的含量明显升高,SOD活性明显降低(P0.05),肾组织bax、Caspase-3蛋白表达明显升高(P0.05),而bcl-2蛋白表达明显降低(P0.05)。与IR组比较,O组血清BUN和Cr的浓度明显降低(P0.05),肾组织MDA的含量明显降低,SOD活性明显升高(P0.05)肾组织bax、Caspase-3蛋白表达明显降低(P0.05),而bcl-2蛋白表达明显升高(P0.05)。结论羟考酮预给药可减轻大鼠肾缺血-再灌注损伤,其机制可能与其抑制肾组织氧化应激反应和细胞凋亡有关。     

The protective effect of ebselen on radiocontrast-induced nephrotoxicity

Aim: Radiocontrast-induced nephropathy has become one of the most important causes of renal acute failure. The most effective management of reducing the incidence of contrast nephropathy is to understand and prevent its causes. We aimed to investigate the protective role of ebselen against radiocontrast-induced nephrotoxicity in terms of tissue oxidant/antioxidant parameters and light microscopy in rats. Methods: Albino Wistar rats were randomly separated into four groups. The Group 1 rats were treated with sodium chloride as the control group, Group 2 with radiocontrast, Group 3 with radiocontrast plus ebselen, and Group 4 with ebselen alone. After 24 h, the animals over the experimental period were euthanized and blood samples were analyzed for blood urea nitrogen (BUN) and serum creatinine (Cr) levels. Kidney sections were analyzed for malondialdehyde (MDA) levels and superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities, as well as histopathological changes. Results: In the radiocontrast group, BUN, MDA, and GSH-Px levels increased while SOD activity decreased compared with the control group. These decays were improved by ebselen administration in the radiocontrast group. Significant histological deteriorations were observed in the radiocontrast group. We noted improvement in the histologic findings with ebselen administration. Conclusion: These results indicate that ebselen might produce a protective mechanism against radiocontrast-induced nephrotoxicity.     

The effect of dexmedetomidine against oxidative and tubular damage induced by renal ischemia reperfusion in rats

Abstract

Dexmedetomidine (dex) is a potent, highly selective and specific α2-adrenoreceptor agonist. This experimental study was designed to investigate protective and therapeutic effect of two different doses of dex, on kidney damage induced by ischemia-reperfusion (I/R) in rats. Male Sprague?Dawley rats were divided into four groups, each including 10 animals: control group, ischemia-reperfusion (I/R) group; treated groups with 10?μg/kg of dex and 100?μg/kg of dex. After removing right kidney of the rats, the left kidney has performed ischemia during 40?min and reperfusion in the following 3?h. The histopathological findings, and also tissue superoxide dismutase (SOD) and catalase (CAT) enzyme activity, malondialdehyde (MDA), glutathione (GSH), serum blood urea nitrogen (BUN), creatinine (Cre) and tumor necrosis factor-alpha (TNF-α) levels were determined. In the I/R group, compared to the control group, levels of BUN, Cre and kidney tissue MDA have increased significantly, SOD, CAT enzyme activity and glutathione levels have decreased significantly. In the dex10 group, compared to the I/R group, levels of Cre and TNF-α have decreased significantly, while the SOD activity has increased significantly. In the dex100 group, compared to the I/R group, levels of BUN, Cre have decreased significantly, while the SOD activity has increased significantly. In the I/R group, there was also extensive tubular necrosis, glomerular damage in the histological evaluation. Dex ameliorated these histological damages in different amounts in two treatment groups. In this study, the protective effects of dex against renal I/R injury have been evaluated by two different amount of doses.     

N-acetylcysteine suppresses colistimethate sodium-induced nephrotoxicity via activation of SOD2, eNOS,and MMP3 protein expressions

Objective: To investigate the molecular mechanisms of colistimethate sodium-induced nephrotoxicity and the protective effect of N-acetylcysteine (NAC) against nephrotoxicity.

Methods: Twenty-eight Wistar rats were divided into four groups comprised of control, colistin, NAC, and colistin–NAC co-treatment, respectively. Serum creatinine and urine N-acetyl-β-d-glucosaminidase (NAG) levels were measured at different time intervals. Histological changes, apoptosis, total oxidant and antioxidant status, and the expression levels of endothelial nitric oxide synthase (eNOS), superoxide dismutase 2 (SOD2), and matrix metalloproteinase 3 (MMP3) were evaluated in renal tissue.

Results: In the colistin group, post-treatment creatinine levels were higher than pretreatment levels (p?=?.001). There was a significant increase in urine NAG level following colistin treatment on day 10, compared to the baseline value and the first day of treatment (p?=?.001 and .0001, respectively). Urine NAG levels were higher in the colistin group on the 10th day of treatment than in the other groups (p?Conclusions: N-acetylcysteine prevented colistin-induced nephrotoxicity through activation of expression levels of SOD2, eNOS, and MMP3.     

Protective role of Diospyros lotus on cisplatin‐induced changes in sperm characteristics,testicular damage and oxidative stress in rats

The aim of this study was to investigate the protective effect of Diospyros lotus (DL) on cisplatin (CP)‐induced testicular damage in male rats. Twenty‐eight male rats were randomly divided into four groups: group 1 – control, given isotonic saline solution; group 2 – CP 7 mg kg⁻¹ given intraperitoneally as single dose; group 3 – DL 1000 mg kg⁻¹ per day given orally for 10 days; group 4 – CP and DL given together at the same doses. CP caused a significant increase in thiobarbituric acid‐reactive substances (TBARS) level and a significant decrease in superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT) and glutathione (GSH) levels in rats testis tissues compared to the control group. CP caused a significant increase in lipid peroxidation in testis tissues compared to the control group, whereas DL led to a significant increase in SOD and GSH levels. However, there were no statistically significant changes in GPx and CAT levels. In addition, serum testosterone levels, sperm concentration and sperm motility were significantly decreased, but abnormal sperm rate and histological changes were increased with CP. However, these effects of CP on sperm parameters, histological changes and the tissue weights were eliminated by DL treatment. In conclusion, our study showed that the reproductive toxicity caused by CP may be prevented by DL treatment.     

Effects of pentoxifylline on gentamicin-induced nephrotoxicity

Abstract

We aimed to investigate the underlying mechanisms responsible for the renoprotective effects of pentoxifylline (PTX) in gentamicin (GEN)-induced nephropathy. On this purpose, 26 female Wistar rats (200–250?g) were included and four groups were formed. The first one was the control group (n:5). The rats in other groups (n:7 for each) received 50?mg/kg twice daily intraperitoneal (i.p.) PTX, 100?mg/kg i.p. GEN and both GEN and PTX at the same doses for consecutive 8 days, respectively. Rats were weighed both at the beginning and end of the study. After the last dose, 24-hour urines were collected and the rats were sacrificed. Blood samples and kidney tissues were obtained for biochemical, histological, oxidative stress, and apoptotic parameters. Body weights were similar in all groups at the beginning of the study. Rats in GEN group had significant weight loss, tubular damage, and increased apoptosis, while GEN?+?PTX group had significantly better outcomes. Scr, urinary protein/creatinine, and TBARS levels were significantly higher and Ccr and SOD levels were significantly lower in GEN and GEN?+?PTX groups in comparison to control and PTX groups, but the levels were similar between GEN and GEN?+?PTX groups. In conclusion, concomitant administration of PTX provides renoprotection via suppressing apoptosis in GEN-induced nephropathy.     

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

Purpose: Pistacia vera is a plant of the family Anacardiaceae found in Central and West Asia. P. vera nut (Pistachio) possess multiple pharmacological effects such as antimicrobial, anti-hyperlipidemia, antioxidant and anti-inflammatory. This study is designed to evaluate the protective effect of the hydroalcoholic extract of pistachio on gentamicin-induced nephrotoxicity in rats.

Methods: Nephrotoxicity was induced in rats by intraperitoneal injection of gentamicin (100?mg/kg/day for 7?days). Hydroalcoholic extract of pistachio (10, 50 and 100?mg/kg/p.o) was administered for 7?days. The nephroprotective activity was evaluated by determining creatinine clearance, serum creatinine, urine volume, urine glucose and blood urea nitrogen (BUN) levels. The kidneys were processed for histopathological examinations and all specimens were examined for morphologic parameters involving tubular degeneration, tubular necrosis and tubule interstitial nephritis.

Results: Results showed a significant increase in the levels of serum creatinine, urine volume, urine glucose and BUN and decrease of creatinine clearance by gentamicin (GA) administration. Co-administration with pistachio extract showed reduction in the levels of serum creatinine, urine volume, urine glucose and BUN and increase of creatinine clearance in all doses but the most significant alteration was observed in doses of 100?mg/kg. Also, the nephroprotective effect of the GA was confirmed by the histological examination of the kidneys.

Conclusion: The study revealed the nephroprotective effect of the hydroalcoholic extract of pistachio. These findings suggest that pistachio treatment may attenuate renal dysfunction and structural damage through the reduction of oxidative stress and inflammation in the kidney.     

Protective effect of aminoguanidine against nephrotoxicity induced by amikacin in rats

Aminoglycoside antibiotics have long been used in antibacterial therapy. Despite their beneficial effects, aminoglycosides have considerable nephrotoxic and ototoxic side effects. It has been reported that reactive oxygen radical species (ROS) play role in the pathophysiology of aminoglycosides-induced nephrotoxicity. Aminoguanidine (AG) is an effective antioxidant and free radical scavenger which has long been known to protect against nephrotoxicity. We investigated the effects of AG on amikacin (AK)-induced changes of renal malondialdehyde (MDA), glutathione (GSH), blood urea nitrogen (BUN), serum creatinine (Cr) and albumin (Alb) which are used to monitor the development of renal tubular damage. Morphological changes in the kidney were also examined using light microscopy. A total of 21 rats were equally divided into three groups which were: (1) injected with saline, (2) injected with AK, and (3) injected with AK+AG, respectively. AK administration to control rats increased renal MDA and decreased GSH levels. AG administration before AK injection caused significant decreases in MDA and increases in GSH levels in kidneys compared to rats treated with AK alone. The serum BUN level increased slightly, Cr and serum Alb did not change as a result of any treatment. AG tended to decrease the level of serum BUN and did not cause any change in Alb or Cr levels. Morphological changes, including glomerular, tubular epithelial alterations and interstitial edema, were clearly observed in AK-treated rats. In addition, AG reversed the morphological damage to the kidney induced by AK. The results show that AG has a protective effect on nephrotoxicity induced by AK and may therefore improve the therapeutic index of AK.     

Selenium has a protective effect on ischemia/reperfusion injury in a rat ovary model: biochemical and histopathologic evaluation

Background/PurposeThe aim of the study was to evaluate the effects of selenium (Se) on ischemia/reperfusion (I/R) injury in rat ovaries.MethodsThirty-five female Sprague-Dawley rats were randomly divided into 5 groups (n = 7): sham (S), I/R1, I/R2, Se1, and Se2. In the I/R1 and Se1 groups, 4 hours of ischemia was followed by 6 hours of reperfusion, and in the I/R2 and Se2 groups, 4 hours of ischemia was followed by 12 hours of reperfusion. In the Se groups, 30 minutes before reperfusion, a single dose of 0.2 mg/kg Se was administered intraperitoneally. The ovarian tissue levels of malondialdehyde (MDA) and nitric oxide (NO), and the activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) were measured biochemically. Tissue damage to ovarian tissue was scored by histopathologic examination.ResultsThe I/R groups had significantly higher MDA levels and lower CAT, SOD, and GPx activities than the sham group (P < .05). Although NO levels were significantly higher in the I/R1 group than in the sham group (P < .05), the NO levels in the I/R2 and sham groups were similar. Selenium pretreatment significantly lowered tissue MDA and NO levels and increased tissue SOD and GPx activities in the Se groups, compared with those in the I/R groups (P < .05). Catalase activities were significantly higher in the Se2 group than in the I/R2 group (P < .05). Catalase activities were higher in the Se1 group than in the I/R1 group, but the difference was not statistically significant. Treatment with Se significantly decreased the ovarian tissue damage scores in the Se2 group compared with those in the I/R2 group (P < .05).ConclusionSelenium is effective in preventing tissue damage induced by I/R in rat ovaries.     

Beneficial effects of aminoguanidine on radiotherapy‐induced kidney and testis injury

This experimental study was designed to investigate both protective and therapeutic effects of aminoguanidine (AG), on radiotherapy (RT)‐induced oxidative stress in kidney and testis. Forty rats were divided into five groups equally as follows: (i) control, (ii) RT, (iii) AG, (iv) AG+RT and (v) RT+AG group. Histopathological findings and biochemical evaluations, including tissue malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX), glutathione (GSH), total oxidant status (TOS), total antioxidant capacity, oxidative stress index (OSI), blood urea nitrogen (BUN), serum creatinine (Cr) and testosterone levels, were determined. MDA, TOS and OSI were significantly higher in RT‐treated groups, whereas SOD, CAT, GPX and GSH were significantly lower in these groups when compared with the control rats in the kidney and testis tissue. AG treatment significantly decreased MDA, TOS and OSI levels and increased SOD, CAT, GPX and GSH levels, when compared to the RT‐treated groups in both kidney and testis tissue. BUN and Cr levels did not change among the groups, whereas testosterone levels were found as reduced in the RT‐treated rats. AG treatment significantly augmented these hazardous effects of RT on testis tissue. According to our results, AG has beneficial effects against RT‐induced kidney and testis injury.     

Effects of pomegranate seed oil on oxidative stress markers,serum biochemical parameters and pathological findings in kidney and heart of streptozotocin-induced diabetic rats

Purpose: Oxidative stress due to hyperglycemia is a major cause of diabetes complications. The aim of this study was to evaluate the effects of pomegranate seed oil (PSO) on serum biochemical parameters, cardiomyopathy and nephropathy induced by diabetes mellitus.

Method: W/A adult rats were divided into four groups (12 each): group 1, received saline (1?mL/kg), group 2, received streptozotocin (STZ, 65?mg/kg, a single dose as i.p.), groups 3 and 4, received STZ?+?PSO (0.4 and 0.8?mL/kg, daily by gavage, respectively). After three weeks, six rats of each group and one week later the remaining animals were anesthetized, blood samples were taken for measuring serum biochemical parameters. Sections of heart and kidneys were used for histopathological studies and the remaining tissues were homogenized for measuring malondialdehyde (MDA) and total sulfhydryl groups.

Results: Significant elevation of serum creatinine and urea, LDL, triglyceride, glucose levels as well as urine markers, MDA levels in tissue homogenates and a significant decrease in total thiol content and serum HDL were observed in STZ-treated group as compared with control group. PSO treatment resulted in a significant decrease in tissue MDA content, serum creatinine and urea levels as well as urine markers as compared with STZ-treated group. Lipid profile was ameliorated with PSO treatment. PSO also significantly reversed STZ-induced depletion in thiol content and histological abnormality. Effect of PSO was more specific at 28th than 21th days of study.

Conclusion: The results showed that PSO has a protective effect against diabetes complications in rats.     

Olive oil abrogates acrylamide induced nephrotoxicity by modulating biochemical and histological changes in rats

Acrylamide (ACR) is one of the most important contaminants occurring in foods heated at high temperatures. The aim of this study is to investigate the protective efficacy of extra virgin olive oil (EVOO), a main component of the Mediterranean diet, against nephrotoxicity induced by ACR. Rats have received by gavage during 21 days either ACR (40?mg/kg body weight) or ACR-associated with EVOO (300?μl) or only EVOO (300?μl). Acrylamide induced nephrotoxicity as evidenced by an increase in malondialdehyde (MDA), hydrogen peroxide (H₂O₂), protein carbonyls (PCOs) and a decrease in glutathione, non-protein thiols (NPSHs), and vitamin C levels. Activities of catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx) were also decreased. Lactate dehydrogenase (LDH) activity, creatinine, urea, and uric acid, urinary volume and creatinine clearance levels were modified. EVOO supplementation improved all the parameters indicated above. Kidney histoarchitecture confirmed the biochemical parameters and the beneficial role of EVOO. EVOO, when added to the diet, may have a beneficial role against kidney injury by scavenging free radicals and by its potent antioxidant power.     

股骨干骨折合并脑损伤后大鼠多器官功能损害的生化指标观察

目的：对大鼠血清中多种生化指标的检测,探讨股骨干骨折合并脑损伤后对大鼠多器官功能的影响。方法：4月龄雄性SD大鼠30只,体重（280±10）g,用随机数字表法将大鼠随机分为对照组,创伤第1天组,创伤第2天组,创伤第3天组,创伤第5天组,创伤第7天组,每组5只。5个创伤组制造大鼠右侧股骨干骨折合并脑损伤的模型,然后分别在造模后第1,2,3,5,7天抽取各组腹主动脉,检测血清中天冬氨酸氨基转移酶（AST）、丙氨酸氨基转移酶（ALT）、肌酐（Cr）、尿素氮（BUN）、乳酸脱氢酶（LDH）、磷酸肌酸激酶（CK）的含量,对照组不做任何处理,只进行上述检测。对各组检测的生化指标进行比较。结果：各组血清中AST、ALT、Cr、BUN、LDH、CK含量差异均有统计学意义（P〈0．01）,其中AST、ALT、BUN、CK在创伤第1天组达到峰值（P〈0．05）;Cr在创伤第3天组达到峰值（P〈0．05）;LDH在创伤第2天组达到峰值（P〈0．05）。结论：股骨干骨折合并脑损伤后会引起大鼠血清中多种生化指标的升高,尤其以创伤后前3d的影响较为显著,这些生化指标改变可间接的反应心、肝、肾器官的功能下降。     

黄芪对梗阻性黄疸大鼠肾功能的保护作用

目的:探讨黄芪对梗阻性黄疸大鼠肾功能的保护作用及机理.方法:SD大鼠胆总管结扎后分2组,每组20只,术后分别用3 mL黄芪或生理盐水腹腔注射.假手术组20只.术后10 d、20 d(每小组n=10)心脏取血测定血浆内皮素(ET-1)、血清超氧化物歧化酶(SOD)和丙二醛(MDA)含量,同时测定血清肌酐(Cr)尿素氮(BUN)和直接胆红素(DB),对肾脏行病理形态学观察.结果:血浆ET-1、血清MDA浓度在梗阻10 d即升高且随胆道梗阻时间延长进一步升高,SOD在梗阻10 d即下降,同时伴有血清Cr、BUN、DB的升高和肾脏病理形态学的进行性改变.黄芪治疗组ET-1及MDA显著低于对照组,而SOD显著高于对照组,并能改善肾组织病理形态.结论:大鼠梗阻性黄疸时血浆ET-1升高及氧自由基损害是肾损伤的原因,黄芪通过降低ET-1水平、抗氧化作用对梗阻性黄疸大鼠肾脏起保护作用.