The effect of exogenous oxytocin on streptozotocin (STZ)-induced diabetic adult rat testes

Aydın, Pınar Koroglu; Şentürk, Gözde Erkanlı; Yucel, D.; Özakpınar, Özlem Bingöl; Uras, Fi̇kri̇ye; Arbak, Serap

doi:10.1016/j.peptides.2014.10.012

Cited by 20 publications

(12 citation statements)

References 29 publications

(19 reference statements)

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“…The STZ group was injected with a single dose of STZ (60 mg/kg, freshly dissolved in 1 mL of saline solution) intraperitoneally for 4 days before surgery. Many other successful STZ administration protocols are described in the literature (2,(28)(29)(30).…”

Section: Discussionmentioning

confidence: 99%

“…Affected individuals require continuous follow-up and suffer numerous disease-related complications. The high levels of blood glucose that characterise DM contribute to an increase in free radical production, enhanced oxidative stress, and changes in antioxidant capacity (1)(2)(3).…”

Section: Introductionmentioning

confidence: 99%

“…By binding to glucose receptors in the plasma membrane, STZ blocks glucose-induced insulin secretion (2,3) and alters blood insulin and glucose concentrations.…”

Section: Introductionmentioning

confidence: 99%

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Effects of Ankaferd BloodStopper on dermal healing in diabetic rats

Aktop¹,

Çevreli²,

Genç³

et al. 2017

Turk J Med Sci

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IntroductionDiabetes mellitus (DM) is a chronic, life-long metabolic disease occurring worldwide. Affected individuals require continuous follow-up and suffer numerous disease-related complications. The high levels of blood glucose that characterise DM contribute to an increase in free radical production, enhanced oxidative stress, and changes in antioxidant capacity (1-3).Streptozotocin (STZ) is the chemical agent most frequently used to induce experimental diabetes in animal models. By binding to glucose receptors in the plasma membrane, STZ blocks glucose-induced insulin secretion (2,3) and alters blood insulin and glucose concentrations.Among the many effects of free radical production is lipid peroxidation (LPO). Oxidation of membrane polyunsaturated fatty acids disrupts cell structure and function and induces cytotoxic, hepatotoxic, mutagenic, and genotoxic effects related to the release of aldehydes (4,5).The tripeptide glutathione (GSH) is found in the cells of all organisms. In humans, GSH concentrations are highest in the liver; in hepatocytes, GSH accounts for 90% of nonprotein sulfhydryl groups. As an important reducing agent and antioxidant, GSH maintains the cellular oxidoreduction balance and protects cells against the toxic effects of oxidants, whether of endogenous or exogenous origin (5-7).Ankaferd BloodStopper (ABS) (Ankaferd Health Products Ltd., İstanbul, Turkey) is a medicinal extract from the plants Thymus vulgaris, Glycyrrhiza glabra, Vitis vinifera, Alpinia officinarum, and Urtica dioica (7,8). ABS is not only an effective haemostatic agent but also Background/aim: Diabetes mellitus inhibits wound-induced angiogenesis, impairs the wound healing process, and leads to the development of chronic wounds. Ankaferd BloodStopper (ABS) is a new and promising local haemostatic agent. Although the mechanism of ABS-mediated haemostasis is well established, little is known about the associated histological and biochemical tissue reactions. The aim of this study was to evaluate the effects of this new-generation local haemostatic agent on short-term soft-tissue healing in streptozotocin (STZ)-treated rats. Materials and methods:The 24 Wistar albino rats used in this study were divided into STZ-treated (STZ, n = 12) and nontreated groups (control, n = 12). Four days prior to surgery, rats in the STZ group were subcutaneously administered 60 mg/kg STZ intraperitoneally, while rats in the control group were administered 1 mL saline/kg. An incision was made in the dorsal dermal tissue of all rats, and either ABS or no haemostatic agent (NHAA) was applied to the wound before suturing. All of the rats were euthanised on postoperative day 4. Blood and skin samples were evaluated biochemically and histologically. Results:The results showed that STZ treatment impaired soft-tissue healing, assessed by measuring glutathione and lipid peroxidation levels. Moreover, while good histological results were obtained in the control group treated with ABS, there were fewer benefits in the STZ-treated group. Conclusion:AB...

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Effects of Ankaferd BloodStopper on dermal healing in diabetic rats

Aktop¹,

Çevreli²,

Genç³

et al. 2017

Turk J Med Sci

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“…Also, alkaloids have also been reported to strongly inhibit lipid peroxidation induced in isolated tissues via its antioxidant activity. The protection offered by the extract could have been due to the presence of flavonoids and alkaloids 48,49 .…”

Section: Effect Of Erml On Anti-oxidant Parametersmentioning

confidence: 99%

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2019

IJPSR

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Oxidative stress has been recommended as a contributory factor in complication and progression of diabetes. The aim of the study was to evaluate the effects of Rhizophora mucronata Leaves on streptozotocin generated oxidative stress induced diabetic nephropathy in rats. Forty Wistar rats were randomly divided into normal control, diabetic untreated and diabetic treated with ethanolic extract of Rhizophora mucronata leaves (ERML) at 250 and 500 mg/kg doses, respectively. Experimental diabetic nephropathy was induced by a single intraperitoneal (i.p) administration of STZ 60 mg/kg body weight (b.w.). The body weight, plasma glucose, creatinine, urea, uric acid as well as total protein along with oxidative stress parameters were investigated in various groups of rats. Histopathological analyses were also conducted on the kidney tissues. In STZ treated rats LPO were increased whereas the level of SOD, CAT and GSH were decreased significantly. ERML at 250 and 500 mg/kg, in a dose-dependent manner, significantly improve all levels as compared to diabetic rats. Destruction of the liver architecture of the hepatocytes in the diabetic group showed the signs of necrosis, degeneration, dilatation, and inflammation in the central vein and blood vessels. In the kidney, shrinkage and lesion in Bowman's capsule were observed. ERML (250 and 500 mg/kg) dose-dependently acted as an antioxidant thereby preventing oxidative damage in the diabetic kidney. INTRODUCTION: Diabetes mellitus is characterized by hyperglycemia resulting from defects in insulin secretion, insulin action, or both. Sustained hyperglycemia is further associated with long-term damage, dysfunction, and failure of various organs and is a major factor in the development of many complications in patients with diabetes 1, 2 .

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“…Although the precise mechanisms involved remain poorly understood, oxidative stress is believed to be one of the major factors contributing to DM. Several previous studies have demonstrated that excessive oxidative stress is generated in response to pancreatic β-cell death in animal models of streptozotocin (STZ)-induced diabetes (5)(6)(7).…”

Section: Introductionmentioning

confidence: 99%

Tat-ATOX1 inhibits streptozotocin-induced cell death in pancreatic RINm5F cells and attenuates diabetes in a mouse model

Ahn

Kim

Shin

et al. 2016

International Journal of Molecular Medicine

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Antioxidant 1 (ATOX1) functions as an antioxidant against hydrogen peroxide and superoxide, and therefore may play a significant role in many human diseases, including diabetes mellitus (DM). In the present study, we examined the protective effects of Tat-ATOX1 protein on streptozotocin (STZ)-exposed pancreatic insulinoma cells (RINm5F) and in a mouse model of STZ-induced diabetes using western blot analysis, immunofluorescence staining and MTT assay, as well as histological and biochemical analysis. Purified Tat-ATOX1 protein was efficiently transduced into RINm5F cells in a dose- and time-dependent manner. Additionally, Tat-ATOX1 protein markedly inhibited reactive oxygen species (ROS) production, DNA damage and the activation of Akt and mitogen activated protein kinases (MAPKs) in STZ-exposed RINm5F cells. In addition, Tat-ATOX1 protein transduced into mice pancreatic tissues and significantly decreased blood glucose and hemoglobin A1c (HbA1c) levels as well as the body weight changes in a model of STZ-induced diabetes. These results indicate that transduced Tat-ATOX1 protein protects pancreatic β-cells by inhibiting STZ-induced cellular toxicity in vitro and in vivo. Based on these findings, we suggest that Tat-ATOX1 protein has potential applications as a therapeutic agent for oxidative stress-induced diseases including DM.

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The effect of exogenous oxytocin on streptozotocin (STZ)-induced diabetic adult rat testes

Cited by 20 publications

References 29 publications

Effects of Ankaferd BloodStopper on dermal healing in diabetic rats

Effects of Ankaferd BloodStopper on dermal healing in diabetic rats

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Tat-ATOX1 inhibits streptozotocin-induced cell death in pancreatic RINm5F cells and attenuates diabetes in a mouse model

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