The Investigation of the Oxidative Stress-Related Parameters in Type 2 Diabetes Mellitus

Aouacheri, O.; Saka, S.; Krim, Meriem; Messaadia, Amira; Maidi, Imen

doi:10.1016/j.jcjd.2014.03.002

Cited by 153 publications

(123 citation statements)

References 34 publications

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“…16 Increased MDA observed in diabetic patients was reported to be attributed to the chronic hyperglycemia that significantly changes oxidative stress markers. 20 In addition, there was significant decrease in CAT, GSH, SOD, GPx levels in serum of untreated diabetic group compared to control one. In a previous study, significant depletion in GSH and GPx content were observed in diabetic patients in comparison with controls.…”

Section: Figure (2)mentioning

confidence: 83%

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Arabic gum acacia improves diabetic peripheral neuropathy in rats: a biochemical and histopathological evidence

Almohaimeed

Amin

El-Aziz

et al. 2018

Int J Basic Clin Pharmacol

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INTRODUCTIONDiabetes mellitus (DM) is thought to be a noteworthy risk to public health. Data from the World Health Organization (WHO) showed that almost half of all deaths attributable to high blood glucose occur before the age of 70 years. WHO projects that diabetes will be the seventh leading cause of death in 2030. 1 Diabetic peripheral neuropathy (DPN) is a frequent complication of diabetes mellitus.Studies conducted in the Middle East revealed high rates of DPN ranged from 35% to 65%. The DPN is more frequently represented than other complications of Diabetes Mellitus. It was reported that it is responsible for 50%-75% of non-traumatic amputations. Painful DPN has high grade of functional disability which influences health-related quality of life. 2 Hyperglycemia is basic for occurrence and advancement of DPN with the etiological hypotheses on metabolic or vascular causes. 3 Regardless of numerous investigations on DPN, the present ABSTRACT Background: Diabetic peripheral neuropathy (DPN) is a frequent complication of diabetes mellitus and unfortunately, its present therapeutic alternatives are exceptionally poor. Objectives of this study was to assess the antidiabetic, antioxidant and hypolipidemic action of Gum Arabic (GA) and its role in promoting the functional recovery from diabetic neuropathy developed in in an experimental model of diabetic neuropathy. Methods: Sixty adult male Sprague-Dawley rats were utilized and randomly assigned into six groups (n= 10); control, Arabic gum-treated, untreated diabetic, diabetic received metformin, diabetic received metformin and B12 vitamin and diabetic received metformin, B12 vitamin and AG. Locomotor activity and hyperalgesia were assed at the end of the study. Fasting and two hours postprandial blood glucose, serum insulin levels, lipid Profile, oxidants/antioxidants parameters were assessed in the blood. Sciatic nerve was assessed histopathologically. Results: The locomotor activity of the untreated diabetic rats was significantly (p<0.001) reduced compared to the control group while it was significantly increased in all treated groups. The lipid profile and Malondialdehyde were significantly improved in all treated groups. Levels of CAT, GSH, SOD, GPx were significantly decreased in untreated diabetic group compared to the control while they were significantly increased in all treated groups compared to the untreated diabetic group. Sciatic nerve fibers of untreated diabetic rats showed degenerated axons with dilated myelin sheaths and degenerated Schwann cells. The nerve had significantly fewer fiber compared to the control. These changes were alleviated in all the treated groups specifically that received metformin, vitamin B12 and GA. Conclusions: It could be concluded that Arabic gum had hypoglycemic, antioxidant and hypolipidemic activity and had a protective effect on diabetic neuropathy. Based on this it is recommended that human clinical trials are necessary to prove this therapeutic effect.

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Section: Figure (2)mentioning

confidence: 83%

“…This depletion was attributed to the chronic hyperglycemia. 20 Hyperglycemia, which leads to cellular tissue damage, was previously reported to induce oxidative stress. 21 In a previous study, Alloxan-induced diabetes caused significant decrease in SOD, CAT, and GPx activities as well as significant increase in MDA production.…”

Section: Figure (2)mentioning

confidence: 99%

Arabic gum acacia improves diabetic peripheral neuropathy in rats: a biochemical and histopathological evidence

Almohaimeed

Amin

El-Aziz

et al. 2018

Int J Basic Clin Pharmacol

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“…Stres oksidatif terjadi karena banyaknya glukosa dalam darah yang menimbulkan autooksidasi glukosa dan membentuk reactive oxygen species (ROS) sebagai radikal bebas. Peningkatan stres oksidatif memicu peningkatan progresivitas diabetes mellitus dengan bersifat reaktif menimbulkan kerusakan sel dan jaringan, meningkatkan kejadian perkembangan komplikasi berupa retinopati, nefropati dan neuropati (Vidya, 2011) (Rochette, 2014) (Aouacheri, 2015). Antioksidan seperti superoksida dismutase (SOD) merupakan enzim yang mampu meredam sifat reaktif ROS dalam tubuh.…”

Section: Pendahuluanunclassified

“…Antioksidan seperti superoksida dismutase (SOD) merupakan enzim yang mampu meredam sifat reaktif ROS dalam tubuh. Aktivitas SOD yang kuat mampu meredam reaktivitas senyawa reaktif pada tubuh sehat, namun produksi ROS yang berlebihan pada diabetes mellitus melemahkan pertahanan SOD dan menimbulkan destruksi sel (Aouacheri, 2015). Penurunan aktivitas enzim antioksidan dapat mengacaukan keseimbangan tubuh akibat reaktivitas ROS.…”

Section: Pendahuluanunclassified

“…(Valle, 2005) (Giacco, 2010) Proses seluler ini menimbulkan stres oksidatif yaitu suatu kondisi akibat ketidakseimbangan antara produksi ROS (sebagai oksidan) dan status antioksidan. (Aouacheri, 2015) (Winarsi, 2012) Pertahanan antioksidan SOD tidak sebanding dengan produksi ROS yang terus menerus pada diabetes sehingga kadar SOD menurun. Sedangkan penurunan SOD kelompok K 1 dapat dikaitkan dengan berat badan tikus yang semakin meningkat.…”

Section: Pembahasan a Pengaruh Zn Terhadap Beratunclassified

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PENGARUH PEMBERIAN Zn TERHADAP KADAR GLUKOSA DARAH DAN KADAR SUPEROKSIDA DISMUTASE PADA TIKUS WISTAR YANG DIINDUKSI STREPTOZOTOCIN

Kartika¹,

Rachmawati

Johan

2016

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Vicenin‐2 inhibits the Helicobacterium pylori infection associated gastric carcinogenic events through modulation of PI3K/AKT and Nrf2 signaling in GES‐1 cells

Zhang

Sun

Dong

et al. 2020

J Biochem & Molecular Tox

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Helicobacter pylori (H. pylori), a microbial carcinogen of Gram‐negative bacteria, has been recognized to be the highest risk factor for the growth of human gastric cancer (GC). Therefore, the inhibition of the growth rate of H. pylori has been considered an effective vital strategy to prevent GC development. This study highlights the inhibitory effect of vicenin‐2 against H. pylori‐induced gastric carcinogen signaling in human gastric epithelial cells (GES‐1). In vitro cytotoxicity studies reported that 40 µM of vicenin‐2 remarkably protects the gastric cells and this concentration shows 85% cell viability also does not produce toxicity. In addition, vicenin‐2 prevents H. pylori‐infected increased depletion of antioxidants mediated by reactive oxygen species generation, DNA damage, malondialdehyde, and nuclear fragmentation. Here, we noticed that vicenin‐2 remarkably suppressed the expression range of the phosphorylated form of phosphatidylinositol 3‐kinase/protein kinase B, phosphorylated p38 kinases, phosphorylated extracellular signal‐regulated kinase‐1, phosphorylated c‐Jun N‐terminal kinase, tumor necrosis factor‐α, interleukin‐6, cyclooxygenase‐2 in GES‐1 infected with H. pylori. Moreover, we observed that vicenin‐2 enhanced the antioxidants protein nuclear factor erythroid factor‐2 and phosphatase and tensin homolog expression in H. pylori‐infected cells. Thus, vicenin‐2 prevents the H. pylori‐associated infection, and its resistance might be a potential strategy in preventing GC induced by H. pylori.

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The Investigation of the Oxidative Stress-Related Parameters in Type 2 Diabetes Mellitus

Abstract: The present study shows that there is an oxidative stress state in type 2 diabetes patients compared with healthy subjects. Our data suggest that chronic hyperglycemia causes a significant change in oxidative stress markers.

Cited by 153 publications

References 34 publications

Arabic gum acacia improves diabetic peripheral neuropathy in rats: a biochemical and histopathological evidence

Arabic gum acacia improves diabetic peripheral neuropathy in rats: a biochemical and histopathological evidence

PENGARUH PEMBERIAN Zn TERHADAP KADAR GLUKOSA DARAH DAN KADAR SUPEROKSIDA DISMUTASE PADA TIKUS WISTAR YANG DIINDUKSI STREPTOZOTOCIN

Vicenin‐2 inhibits the Helicobacterium pylori infection associated gastric carcinogenic events through modulation of PI3K/AKT and Nrf2 signaling in GES‐1 cells

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