Effects of captopril on the cysteamine-induced duodenal ulcer in the rat

Saghaei, F; Karimi, Iraj; Jouyban, Abolghasem; Samini, Morteza

doi:10.1016/j.etp.2010.10.001

Cited by 26 publications

(16 citation statements)

References 19 publications

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“…Importantly, vanin-1 has been found to be involved in oxidative stress and inflammatory processes by releasing cysteamine [48], which suppresses the activity of antioxidants including SOD and GSH, thereby creating oxidative stress status [16]. In addition, vanin-1-deficient mice displayed cysteamine activity loss with subsequent activation of γ-glutamylcysteine synthetase that leads to elevated GSH stores, an important protecting enzyme against oxidative stress-induced tissue damage [50].…”

Section: Discussionmentioning

confidence: 99%

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Amelioration of Early Markers of Diabetic Nephropathy by Linagliptin in Fructose-Streptozotocin-Induced Type 2 Diabetic Rats

Oraby

El-Yamany

Safar

et al. 2019

Nephron

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Background: Early prediction and clinical intervention are extremely important in order to delay or hinder diabetic nephropathy (DN) progression. Objectives: This study aimed to detect early signs of DN and study the potential ameliorating effect of the dipeptidyl peptidase-4 inhibitor, linagliptin, on some early markers for DN in fructose-streptozotocin (Fr-STZ)-induced diabetic rats. Method: Fr-STZ rats were treated with either linagliptin (3 mg/kg p.o. daily), metformin (350 mg/kg p.o. daily), or their combination for 6 weeks. Results: Fr-STZ DN rats exhibited obvious tubular renal damage and glomerular podocyte injury as confirmed by renal kidney injury molecule-1 (KIM-1), neutrophil gelatinase-associated lipocalin (NGAL), and vanin-1 mRNA, as well as urinary N-acetyl-β-D-glucosaminidase elevation and nephrin mRNA suppression, associated with the appearance of marked renal interstitial fibrosis and glomerulosclerosis despite the absence of microalbuminuria. Initiation of oxidative, inflammatory, fibrotic, and apoptotic reactions was evident in the settings of renal hyperglycemia. Linagliptin significantly modulated the aforementioned renal tubular injury makers and restored glomerular nephrin expression as well as reversed renal histopathological alterations. Oxidative, inflammatory, fibrotic and apoptotic processes were also alleviated. Conclusions: This study suggests that linagliptin exerts renoprotection against early features of DN in rats probably by inhibition of high glucose-induced renal tubular and glomerular injury thereby hampering KIM-1 and NGAL as well as vanin-1 associated with renal inflammation, fibrosis and oxidative stress.

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Section: Discussionmentioning

confidence: 99%

“…Vanin-1 is an epithelial ectoenzyme that activates the conversion of pantetheine into pantothenic acid (vitamin B5) and cysteamine [15], the latter has been found to inhibit the activity of the antioxidant superoxide dismutase (SOD) and glutathione (GSH), allowing free radicals to promote oxidative tissue damage [16].…”

Section: Introductionmentioning

confidence: 99%

Amelioration of Early Markers of Diabetic Nephropathy by Linagliptin in Fructose-Streptozotocin-Induced Type 2 Diabetic Rats

Oraby

El-Yamany

Safar

et al. 2019

Nephron

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“…Vanin‐1 is an epithelial glycosylphosphatidylinositol (GPI)‐anchored pantetheinase, which catalyzes the conversion of pantetheine into pantothenic acid (vitamin B5) and cysteamine . Cysteamine may decrease the protective activities of superoxide dismutase (SOD) and glutathione peroxidase (GSHPx) against reactive oxygen species (ROS) toxicity, allowing free radical production to overwhelm antioxidant defense systems . Thus, vanin‐1 is involved in oxidative stress in tissues.…”

Section: Introductionmentioning

confidence: 99%

Early urinary biomarkers of renal tubular damage by a high‐salt intake independent of blood pressure in normotensive rats

Washino

Hosohata

Jin

et al. 2017

Clin Exp Pharma Physio

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Dietary sodium intake has been associated with progression to chronic kidney disease (CKD) as well as hypertension. A high-salt intake causes renal damage independent of hypertension. Because traditional renal biomarkers are insensitive, it is difficult to detect renal injury induced by a high-salt intake, especially in normotensive patients. Here, we investigated whether newly developed renal biomarkers could be detected earlier than traditional biomarkers under a high-salt intake, in normotensive rats. Male Wistar Kyoto rats (WKY) received a regular (0.8% NaCl) or salt-loaded (2, 4, and 8% NaCl) diet from 9 to 17 weeks of age. A urine sample was obtained once a week and urinary vanin-1, neutrophil gelatinase-associated lipocalin (NGAL), and kidney injury molecule-1 (Kim-1) were measured. At 17 weeks of age, 8% salt-loaded WKY showed histopathological renal tubular damage and elevated Rac1 activity in renal tissues. Although there was no significant increase in serum creatinine, urinary albumin, N-acetyl-β-D-glucosaminidase (NAG), or Kim-1 during the study period among the groups, urinary vanin-1 and NGAL significantly increased in 8% salt-loaded WKY from 10 to 17 weeks of age. These results suggest that urinary vanin-1 and NGAL, which might be induced by salt per se, are potentially earlier biomarkers for renal tubular damage in normotensive rats under a high-salt intake.

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“…New studies propose that it may also acts as a scavenger of free radicals because of its thiol group [1,2].…”

Section: Introductionmentioning

confidence: 99%

Preparation of a manganese titanate nanosensor: Application in electrochemical studies of captopril in the presence of para-aminobenzoic acid

Ghoreishi

Karamali

Khoobi

et al. 2015

Analytical Biochemistry

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Effects of captopril on the cysteamine-induced duodenal ulcer in the rat

Cited by 26 publications

References 19 publications

Amelioration of Early Markers of Diabetic Nephropathy by Linagliptin in Fructose-Streptozotocin-Induced Type 2 Diabetic Rats

Amelioration of Early Markers of Diabetic Nephropathy by Linagliptin in Fructose-Streptozotocin-Induced Type 2 Diabetic Rats

Early urinary biomarkers of renal tubular damage by a high‐salt intake independent of blood pressure in normotensive rats

Preparation of a manganese titanate nanosensor: Application in electrochemical studies of captopril in the presence of para-aminobenzoic acid

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