Protective Effects of Glurenorm (Gliquidone) Treatment on the Liver Injury of Experimental Diabetes

Yanardağ, Refiye; Saçan, Özlem; Orak, Haci; Ozgey, Yasemin

doi:10.1080/01480540500262961

Cited by 12 publications

(9 citation statements)

References 47 publications

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“…Various means of preventing this increase have been investigated both in vitro and in vivo. It has been reported that various plant extracts [40,41], oral antidiabetic drugs [26], vitamin [42], and trace elements such as vanadium [43] and zinc [44] prevent the increase of tissue NEG levels [45]. In this study, the increase in NEG levels in liver tissue was considerably lowered by the combination of vitamin C, vitamin E, and Se.…”

Section: Discussionmentioning

confidence: 55%

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The Effects of Combined Treatment of Antioxidants on the Liver Injury in STZ Diabetic Rats

et al. 2008

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The aim of this study was to examine whether an antioxidant combination of vitamin C, vitamin E, and sodium selenate (Se) has an effect on the liver of diabetic rats. Vitamin C, vitamin E, and Se were administered for 30 days to streptozotocin (STZ)-induced diabetic and control groups. In the STZ diabetic group, blood glucose levels, liver lipid peroxidation (LPO), and nonenzymatic glycosylation (NEG) levels increased, but blood and liver glutathione levels decreased. On the other hand, combined antioxidant treatment reversed these effects. In the diabetic group, some degenerative changes were observed by light and electron microscopic examinations, but the degenerative changes decreased in the diabetic group given antioxidant combination. Proliferating cell nuclear antigen (PCNA) immunohistochemistry showed that the number of proliferative hepatocytes increased significantly with antioxidant treatment. It was concluded that combined treatment with vitamin C, vitamin E, and Se has a curative effect against the hepatotoxicity produced by STZ-induced diabetes.

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Section: Discussionmentioning

confidence: 55%

“…During diabetes, we observed a significant decrease in GSH levels in liver tissue. In a similar manner, previous study have reported that there was a decreament in the liver GSH level of diabetic rats [26]. The decreased GSH levels represent increased utilization due to oxidative stress [27].…”

Section: Discussionmentioning

confidence: 77%

The Effects of Combined Treatment of Antioxidants on the Liver Injury in STZ Diabetic Rats

et al. 2008

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“…During the early onset of diabetes, oxidative stress occurs and progressively increases. Increased oxidative stress is believed to play a crucial role in the aetiology and pathogenesis of chronic complications of diabetes in diverse tissues . The link has been described between oxidative stress and the pathological alterations in liver morphology and function that are observed in diabetes .…”

Section: Mechanisms Involved In the Development Of Diabetic Liver Injurymentioning

confidence: 99%

Role of stem cells during diabetic liver injury

Wan

Garner

et al. 2015

J Cellular Molecular Medi

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Diabetes mellitus is one of the most severe endocrine metabolic disorders in the world that has serious medical consequences with substantial impacts on the quality of life. Type 2 diabetes is one of the main causes of diabetic liver diseases with the most common being non‐alcoholic fatty liver disease. Several factors that may explain the mechanisms related to pathological and functional changes of diabetic liver injury include: insulin resistance, oxidative stress and endoplasmic reticulum stress. The realization that these factors are important in hepatocyte damage and lack of donor livers has led to studies concentrating on the role of stem cells (SCs) in the prevention and treatment of liver injury. Possible avenues that the application of SCs may improve liver injury include but are not limited to: the ability to differentiate into pancreatic β‐cells (insulin producing cells), the contribution for hepatocyte regeneration, regulation of lipogenesis, glucogenesis and anti‐inflammatory actions. Once further studies are performed to explore the underlying protective mechanisms of SCs and the advantages and disadvantages of its application, there will be a greater understand of the mechanism and therapeutic potential. In this review, we summarize the findings regarding the role of SCs in diabetic liver diseases.

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“…Yarat et al [14] demonstrated that gliquidone markedly lowered the level of nonenzymatic glycosylation protein and total protein and increased the level of lens glutathione in diabetic rats. Yanardag et al [15] reported that gliquidone lessened the STZ-induced hepatic lesions by reducing oxidative stress in diabetic rats. In patients with diabetic nephropathy, substitution of oral glibenclamide with gliquidone has increased the glomerular filtration rate and lowered urinary albumin [16].…”

Section: Introductionmentioning

confidence: 99%

Gliquidone Alleviates Diabetic Nephropathy by Inhibiting Notch/Snail Signaling Pathway

Tian

Yang

Xie

et al. 2018

Cell Physiol Biochem

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Background/Aims: Diabetic nephropathy is a common complication of diabetes. This study explored the renal protective effect and possible mechanism of gliquidone in mice with diabetic nephropathy. Methods: Animal model of diabetic nephropathy was established in KKAy mice. The renal protective effect of gliquidone was studied by evaluating the kidney function through measures of urinary protein, blood urea nitrogen (BUN), serum creatinine (Scr) and serum triglyceride (TG) that were performed using an automatic biochemical analyzer. The levels of oxidative stress indicators, such as nitric oxide (NO), superoxide dismutase (SOD) and malondialdehyde (MDA), were evaluated in renal tissue homogenates using the automatic biochemical analyzer. The inhibitory effect of gliquidone on renal interstitial fibrosis and its association with Notch / Snail1 signaling pathway in diabetic nephropathy was investigated using molecular biological techniques. Results: It was found that low-, medium- and high-dose gliquidone improved the mice’s general health condition, such as mental status, fur condition, eating, and drinking. Gliquidone reduced the body weight and the kidney weight /body weight ratio of mice. Gliquidone improved the kidney function, indicated by reductions in urinary protein, blood urea nitrogen, and serum creatinine and triglyceride. Gliquidone treatment increased levels of nitric oxide and superoxide dismutase, but decreased level of malondialdehyde. The expression of Jagged1/Notch1/hes1/Snail1/α-SMA decreased, while the expression of E-cadherin increased in gliquidone-treated kidneys. High dose gliquidone showed the best effect, one that was similar to that of the positive control drug irbesartan. Conclusion: Taken together, our results suggested that gliquidone can ameliorate the diabetic symptoms of diabetic nephropathy through inhibiting Notch / Snail1 signaling pathway, improving anti -oxidative response and delaying renal interstitial fibrosis. The efficacy of gliquidone is dose-dependent.

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Protective Effects of Glurenorm (Gliquidone) Treatment on the Liver Injury of Experimental Diabetes

Cited by 12 publications

References 47 publications

The Effects of Combined Treatment of Antioxidants on the Liver Injury in STZ Diabetic Rats

The Effects of Combined Treatment of Antioxidants on the Liver Injury in STZ Diabetic Rats

Role of stem cells during diabetic liver injury

Gliquidone Alleviates Diabetic Nephropathy by Inhibiting Notch/Snail Signaling Pathway

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