The combined effect of metformin and l-cysteine on inflammation, oxidative stress and insulin resistance in streptozotocin-induced type 2 diabetes in rats

Salman, Zenat K.; Refaat, Rowaida; Selima, Eman; Sarha, Ashgan El; Ismail, Menna A.

doi:10.1016/j.ejphar.2013.07.002

Cited by 70 publications

(40 citation statements)

References 59 publications

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“…Furthermore, persistent hyperglycemia caused by alloxan injection causing oxidative stress which resulting in further damage of pancretic β-cells which have intrinsically low antioxidant enzymes defense in a phenomenon called glucose toxicity (Robertson et al, 2004). Treatment with metformin resulted in a remarkable preservation of pancretic β-cells from further damage by oxidative stress as a result of its hypoglycemic effect in agreement with Salman et al (2013). Also, ginseng-treated group showed moderate ameliorative effect on hyperglycemic β-cells damage and the possible explanation may be that ginseng has been shown to exhibit an anti-apoptotic function on pancreatic β-cells via regulation of nitric oxide and reactive oxygen species production (ROS scavenging) (Kim and Kim, 2008).…”

Section: Fig (1): Hande Stained Sections Of Pancreas Of Rat Of (A)-diabsupporting

confidence: 60%

The Effect of Metformin and Ginseng on Alloxan-Induced Diabetic Rats: Hematological, Biochemical and Histopathological Studies

El-Karim¹,

Oda²,

Tohamy³

et al. 2017

AJVS

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Section: Fig (1): Hande Stained Sections Of Pancreas Of Rat Of (A)-diabsupporting

confidence: 60%

The Effect of Metformin and Ginseng on Alloxan-Induced Diabetic Rats: Hematological, Biochemical and Histopathological Studies

El-Karim¹,

Oda²,

Tohamy³

et al. 2017

AJVS

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“…The direct anti-inflammatory action of metformin has been reported in several animal experimental studies, both in the liver (69,54,47) and in circulating polymorphonuclear cells (9). In contrast to these experimental findings, metformin efficiency in human NASH treatment is the subject of open debate (58,60).…”

Section: Discussionmentioning

confidence: 73%

Metformin prevents ischemia reperfusion-induced oxidative stress in the fatty liver by attenuation of reactive oxygen species formation

Cahová

Páleníčková

Daňková

et al. 2015

American Journal of Physiology-Gastrointestinal and Liver Physi

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Z, Oliyarnyk O, Kazdova L. Metformin prevents ischemia reperfusion-induced oxidative stress in the fatty liver by attenuation of reactive oxygen species formation. Am J Physiol Gastrointest Liver Physiol 309: G100 -G111, 2015. First published June 4, 2015; doi:10.1152/ajpgi.00329.2014.-Nonalcoholic fatty liver disease is associated with chronic oxidative stress. In our study, we explored the antioxidant effect of antidiabetic metformin on chronic [high-fat diet (HFD)-induced] and acute oxidative stress induced by short-term warm partial ischemia-reperfusion (I/R) or on a combination of both in the liver. Wistar rats were fed a standard diet (SD) or HFD for 10 wk, half of them being administered metformin (150 mg·kg body wt Ϫ1 ·day Ϫ1 ). Metformin treatment prevented acute stress-induced necroinflammatory reaction, reduced alanine aminotransferase and aspartate aminotransferase serum activity, and diminished lipoperoxidation. The effect was more pronounced in the HFD than in the SD group. The metformin-treated groups exhibited less severe mitochondrial damage (markers: cytochrome c release, citrate synthase activity, mtDNA copy number, mitochondrial respiration) and apoptosis (caspase 9 and caspase 3 activation). Metformin-treated HFD-fed rats subjected to I/R exhibited increased antioxidant enzyme activity as well as attenuated mitochondrial respiratory capacity and ATP resynthesis. The exposure to I/R significantly increased NADH-and succinate-related reactive oxygen species (ROS) mitochondrial production in vitro. The effect of I/R was significantly alleviated by previous metformin treatment. Metformin downregulated the I/R-induced expression of proinflammatory (TNF-␣, TLR4, IL-1␤, Ccr2) and infiltrating monocyte (Ly6c) and macrophage (CD11b) markers. Our data indicate that metformin reduces mitochondrial performance but concomitantly protects the liver from I/R-induced injury. We propose that the beneficial effect of metformin action is based on a combination of three contributory mechanisms: increased antioxidant enzyme activity, lower mitochondrial ROS production, and reduction of postischemic inflammation. metformin; oxidative stress; mitochondrial respiration; liver injury; 31 P MR spectroscopy METFORMIN IS AN ORAL ANTIHYPERGLYCEMIC drug widely used in the treatment of Type 2 diabetes (T2D) (7). There is evidence that metformin also protects against oxidative stress in various tissues, although the antioxidant activity of metformin is not well understood. It has been shown that hyperglycemia is associated with increased reactive oxygen species (ROS) formation due to superoxide overproduction from the mitochondrial electron transport chain as a consequence of increased glycolysis (8). It has been hypothesized that the antioxidative effect of metformin is simply the consequence of its glucoselowering effect and subsequent decrease in superoxide anion production (3). Nevertheless, metformin has also displayed antioxidative characteristics in several models of oxidative stress without hyperglycemia (2,19,20,2...

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“…The antihyperglycemic properties of metformin are mainly attributed to its suppression of hepatic glucose production, especially hepatic gluconeogenesis, and slightly increased peripheral tissue insulin sensitivity 4 . MET, independent of its antidiabetic effect, was reported to offer protection against vascular and other inflammatory complications 5 .…”

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confidence: 99%

Modulatory Effect of Lovastatin on Therapeutic Efficiency of Conventional Antidiabetics on Pancreatic and Cardiovascular Complications of Diabetes

El-Shoura

Messiha

Abo-Youssef

et al. 2015

PBJ

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The aim of the present study is to assess the possible modulatory effect of lovastatin (LOVA) on metformin (MET) and gliclazide (GLIC) on pancreatic and cardiovascular complications in rats with experimentally induced diabetes. Male Swiss rats were randomly assigned to seven groups.Group 1 served as normal control group. Group 2 served as diabetic control group, treated with streptozotocin (STZ) alone. Groups 3, 4, 5, 6 and 7 received LOVA, MET, GLIC, LOVA plus MET and LOVA plus GLIC, respectively, for 30 consecutive days after treatment with STZ. To evaluate the modulatory effect of LOVA, blood glucose level was assessed coupled with pancreatic tissue levels of oxidative stress markers including thiobarbituric acid reactive substances (TBARS) production, glutathione reduced (GSH) stores, total nitrite (NO2 -) production as well as glutathione-S-transferase (GST), superoxide dismutase (SOD) and catalase (CAT) activities.Degree of lipid derangement was evaluated by measuring serum levels of 3-hydroxy-3-

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The combined effect of metformin and l-cysteine on inflammation, oxidative stress and insulin resistance in streptozotocin-induced type 2 diabetes in rats

Cited by 70 publications

References 59 publications

The Effect of Metformin and Ginseng on Alloxan-Induced Diabetic Rats: Hematological, Biochemical and Histopathological Studies

The Effect of Metformin and Ginseng on Alloxan-Induced Diabetic Rats: Hematological, Biochemical and Histopathological Studies

Metformin prevents ischemia reperfusion-induced oxidative stress in the fatty liver by attenuation of reactive oxygen species formation

Modulatory Effect of Lovastatin on Therapeutic Efficiency of Conventional Antidiabetics on Pancreatic and Cardiovascular Complications of Diabetes

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