This study was the first to evaluate the possible protective effects of cinnamic acid (CA) against Gentamicin (GM) induced liver and kidney dysfunctions in rats. Adult male Wistar rats were randomly assigned to 4 equal groups (n ¼ 8): Control group (saline, 0.5 ml/day), CA group (CA, 50 mg/kg/day), GM group (GM, 100 mg/kg/day), and GM þ CA group (100 & 50 mg/kg/day). Following 12 days of treatments, blood and 24 h urine samples were collected and kidneys were taken out for biochemical, histopathological, and molecular studies. Following CA treatment, renal function markers and transaminases activities including serum urea (59.92%) and creatinine (50.41%), protein excretion rate (43.67%), and serum activities of aspartate aminotransferase (AST) (54.34%) and alanine aminotransferase (ALT) (47.26%) significantly reduced in the treated group as compared with the GM group (P < 0.05). Also, CA could significantly ameliorate the levels of triglyceride (29.70%), cholesterol (13.02%), very low-density lipoprotein (29.69%) and high-density lipoprotein-cholesterol (7.28%). CA could also attenuate oxidative stress through a decrease of serum malondialdehyde (MDA) (50.86%) and nitric oxide (NO) (0.85%) and an increase of renal catalase (CAT) (196.14%) and glutathione peroxidase (GPX) activities (45.88%) as well as GPX mRNA expression (44.42-fold) as compared with the GM group (P < 0.05). Moreover, histopathological evaluations revealed attenuated tubular damages and reduced inflammatory cellular infiltration in CA treated animals. Overall, CA alleviates GM-induced nephrotoxicity and alterations in transaminases activities in rats through its antioxidant activities.

Gallic acid (GA), as a strong antioxidant, was selected in this study to investigate its possible nephroprotective effects against gentamicin (GM)-induced nephrotoxicity. Twenty-four rats were separated into three groups (n=8): group 1 (control group) received saline (0.5 mL/day), group 2 (GM group) received GM (100 mg/kg/day), and group 3 (treated group) received GM (100 mg/kg/day) and GA (100mg/kg/day). All treatments were performed intraperitoneally for 12 days. After 12 days, the rats were euthanized, and kidneys were removed immediately. For serum preparation, blood samples were collected before killing. Kidney paraffin sections were prepared from one of the kidneys and stained by the periodic acid-Schiff process. GA significantly decreased GM-induced renal histopathological injuries, including tubular necrosis, tubular cast, and leucocyte infiltration compared with the GM group. Additionally, GA significantly improved proteinuria, serum levels of urea and creatinine, and serum activities of aspartate aminotransferase (AST) and alanine HIGHLIGHTS  Gallic acid ameliorates gentamicin-induced nephrotoxicity.  Gallic acid decreases levels of NO and MDA and enhances abilities of GSH, GPX, and CAT.  Gallic acid improves altered liver and renal function markers in nephrotoxic animals.  Gallic acid reduces renal histopathological injuries.  2 Ahmadvand, H.; et al.

Introduction: Methotrexate (MTX), used in the treatment of cancerous patients, causes toxicity in the different organs of the body. This study of rosmarinic acid (RA) is as an antioxidant on nephrotoxicity and hepatotoxicity induced by MTX. Methods: Rats (n = 32) were divided into four groups: sham; MTX; 100 mg\kg RA + MTX; 200 mg/kg RA + MTX. The amount of MTX was 20 mg/kg. 24 hours after injection of the last dose of MTX, the blood samples and kidneys and liver of rats were studied. The aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), urea, serum creatinine were assessed. Tissue antioxidant enzymes and malondialdehyde (MDA) levels were measured. The liver and kidney tissues were histopathologically examined. Results: MTX significantly increased the urea, creatinine, ALT, AST, ALP levels, and renal MDA and significantly decreased renal catalase (CAT), hepatic glutathione (GSH), and hepatic CAT activity. MTX induced necrosis, leukocyte infiltration, eosinophilic casts, glomerular damage in kidney tissue and necrosis, degeneration and cellular vacuolization in liver tissues. RA at 100 mg/kg caused a significant decrease in ALT and AST and at two doses significantly decreased urea, renal MDA, and liver MDA. RA at 200 mg/kg significantly increased the renal CAT and liver GSH. RA in two doses significantly decreased necrosis and Leukocyte infiltration. RA caused a significant decrease in degeneration and cellular vacuolization in liver tissues. Conclusions: RA with its antioxidant and anti-inflammatory characteristics decreased the MTX induced nephrotoxicity and hepatotoxicity.

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Background It has been indicated that Angiotensin-Converting Enzyme Insertion/Deletion (ACE I/D) polymorphism (rs4646994) could be regarded as a genetic factor that raises the risk of CAD through its impact on the activity of Angiotensin-Converting Enzyme (ACE) and angiotensin II level. The present study seeks to examine the relationship between ACE I/D polymorphism with the risk of atherosclerosis. Moreover, its potential effects on ACE activity and oxLDL level are investigated. Methods In this study, 145 healthy individuals and 154 patients (143 males and 156 females) were selected among the subjects referred to Shahid Madani Hospital. Atherosclerosis was determined in all subjects with gold standard angiography. Blood samples were collected, used to isolate white blood cells (WBC) and serum separation. The DNA was extracted and the polymorphism was determined by polymerase chain reaction (PCR). The enzyme activity was measured using high-performance liquid chromatography (HPLC). Results This study indicated that patients with atherosclerosis had higher levels of oxidized Low-Density Lipoprotein (oxLDL) and ACE activity ( P < 0.05) as compared to controls. Although we found a significant association between ACE I/D polymorphism genotype and the allele with atherosclerosis in the male group, there were no association when the entire patient group was compared to the entire control group. Conclusion Our study revealed the ACE I/D polymorphism of the ACE gene may not be an independent risk factor in the development of atherosclerosis and evaluation of ACE activity level is more important in evaluating the risk of disease. The researchers found no relation between ACE I/D polymorphism and atherosclerosis and also between types of genotype, ACE activity, and OxLDL level.