scholarly journals Antioxidant Protection by American Ginseng in Pancreatic ß-Cells

2008 ◽  
Vol 36 (05) ◽  
pp. 981-988 ◽  
Author(s):  
Elaine Lin ◽  
Yong Wang ◽  
Sangeeta Mehendale ◽  
Shi Sun ◽  
Chong-Zhi Wang ◽  
...  

Hyperglycemia in diabetic conditions may cause oxidative stress in pancreatic ß-cells, leading to their dysfunction and insulin resistance within peripheral tissues. Previous studies suggest that American ginseng berry extract may have hypoglycemic effects, as well as offer antioxidant protection. We examined effects of American ginseng berry extract and ginsenoside Re in a pancreatic ß-cell line, MIN-6, to determine if these two properties are related. Cells were exposed to oxidative stress via hydrogen peroxide incubation and oxidative stress was measured by oxidation of 2′,7′-dichlorofluorescin diacetate. These cells showed a concentration-related response to hydrogen peroxide at 100–500 μM. In acute conditions where cells were treated with the extract for 10 min, we observed reduced oxidant injury suggesting direct scavenging effects. Chronic incubation of cells with the extract for 48 hours also demonstrated attenuation of oxidative stress. At high concentrations, Re showed a mild antioxidant effect in MIN-6 cells. Our insulin release observations also showed that the extract may help to increase insulin secretions from the cells. Our data suggest that the observed ability of ginseng to reduce blood glucose levels may be linked to its antioxidant effects on pancreatic ß-cells.

The aim of this study was to investigate the peroxidase activity of Hb with different concentrations of hydrogen peroxide and compare it with hypochlorous acid effect on Hb. Hypochlorous acid at higher concentrations decomposed Hb and heme, releasing fee iron ion from the metal center. High concentrations of hydrogen peroxide switched the peroxidase activity of Hb towards the partial Hb and heme destruction. Heme alone was degraded showing that the Hb conformation and protein environment protects Hb from the distraction in the presence of highly increased hydrogen peroxide concentration that occurs as a result of oxidative stress. In the presence of CT-DNA acted inhibition of the peroxidase activity of Hb was observed signaling inhibited hydrogen peroxide consumption.


2021 ◽  
Author(s):  
Yulia Abalenikhina ◽  
◽  
Elena A. Sudakova ◽  
Pelageya Erokhina ◽  
Aleksey Shchulkin ◽  
...  

The article discusses the new role of pregnane X receptor (PXR) under conditions of oxidative and nitrosative stress. The results showed that the effect of hydrogen peroxide and S-nitrosoglu-tathione in high concentrations on Caco-2 cells leads to a decrease in cell viability, which is accompanied by an increase in the amount of PXR. These changes are offset by the addition of ketoconazole (inhibitor of PXR) to the medium.


2020 ◽  
Vol 6 (3) ◽  
pp. 149
Author(s):  
Indi Kamilia Fitri ◽  
Cholis Abrori ◽  
Dion Krismashogi Dharmawan

In people with diabetes mellitus (DM) there is a decrease in basal vitamin C levels which is thought to be a result of oxidative stress in the condition of hyperglycemia that it needs to increase vitamin C as an antioxidant. Hyperglycemia in DM needs to be lowered by pharmacological therapy, named glimepirid so the purpose of this study is to determine the effectiveness of vitamin C addition to the reduction of KGD hyperglycemic mice with glimepirid treatment. This study is true experimental with a sample of 25 mice 20-30 grams and divided into five groups, first the control group (K0); STZ  induction group (K1); STZ induction group with glimepirid treatment (K2); STZ induction group with the treatment of vitamin C (K3); STZ induction group by treatment of a combination of glimepirid and vitamin C (K4). STZ is injected intraperitonially 150 mg / kgBB. All groups were measured for KGD 1 after induction of STZ and KGD 2 after treatment for fourteen days. The results of the STZ induction group with the treatment of a combination of glimepirid and vitamin C (K4) experienced a smaller and not significant decrease in BSL in the STZ induction group with a single glimepirid (K2) treatment. These results are thought to have an influence from interactions between drugs that cause one drug to not work optimally. The conclusion of this study is that administration of glimepirid, vitamin C, or both can reduce blood glucose levels in hyperglycemic mice with the greatest decrease occurring in the glimepirid group.


2020 ◽  
Vol 21 (23) ◽  
pp. 9149
Author(s):  
Céline Ransy ◽  
Clément Vaz ◽  
Anne Lombès ◽  
Frédéric Bouillaud

Addition of hydrogen peroxide (H2O2) is a method commonly used to trigger cellular oxidative stress. However, the doses used (often hundreds of micromolar) are disproportionally high with regard to physiological oxygen concentration (low micromolar). In this study using polarographic measurement of oxygen concentration in cellular suspensions we show that H2O2 addition results in O2 release as expected from catalase reaction. This reaction is fast enough to, within seconds, decrease drastically H2O2 concentration and to annihilate it within a few minutes. Firstly, this is likely to explain why recording of oxidative damage requires the high concentrations found in the literature. Secondly, it illustrates the potency of intracellular antioxidant (H2O2) defense. Thirdly, it complicates the interpretation of experiments as subsequent observations might result from high/transient H2O2 exposure and/or from the diverse possible consequences of the O2 release.


2019 ◽  
Vol 59 (9) ◽  
pp. 106-109
Author(s):  
Ksenia A. Zagorodnikova ◽  

Paracetamol (acetaminophen, APAP) is a commonly-used antipyretic and analgesic. However, there have been reports indicating possible link between its use in pregnancy and impaired neuropsychic development in children. A number of prospective studies of the possible negative effect of acetaminophen on the development of a child after his mother took this drug during pregnancy, as well as the results of studies on glioma cells and neurons in murine cortex, may indicate presence of the neurotoxic effect of acetaminophen. It is currently unclear if paracetamol itself being pharmacologically active neurotropic substance, or its metabolites, one of which – NAPQI (N-acetyl-p-benzoquinone imine) known by its toxic effects in mitochindria, play the most significant role in proposed neurotoxicity. Therefore it seems important to study each metabolite separately. The ability of acetaminophen(paracetamol) in concentrations of 1 mg/ml and 2 mg/ml to reduce cell viability was shown on cells of the PC12 neuronal line using MTT-method, which is based on the ability of mitochondria of viable cells to restore formazan 3-(4,5-dimethylthiazole)-2,5-diphenyl-2-tetrazolium bromide (MTT). Concentrations of 0.125 mg/ml, 0.25 mg/ml and 0.5 mg/ml had no similar impact on cell culture viability. In addition, the impact of hydrogen peroxide (as an inducer of oxidative stress) on the neurotoxic effect of acetaminophen was studied. We demonstrated that in the presence of 0.3 mM or 0.5 mM hydrogen peroxide and acetaminophen in concentrations of 1 mg/ml and 2 mg/ml reliably reduced the percentage of surviving cells. We showed that the decrease of the viability of the cells of the PC12 neuronal line is obvious only after exposure to high concentrations of acetaminophen, especially in the presence of hydrogen peroxide, which means that neurotoxic effect is not likely to occur in vivo.


Author(s):  
B. Fenton-Navarro ◽  
MV. Urquiza Martínez ◽  
BB. Fiscal Castro ◽  
OI. Medrano Castillo ◽  
M. López-Rodríguez ◽  
...  

Background: Watercress is a semi-aquatic plant used in traditional medicine to treat various ailments, such as flu, cough, avitaminosis, and anorexia; it is also used as a diuretic and for hypoglycemia treatment in diabetes. In this study, we report the antioxidant and hypoglycemic activity of orally administered aqueous (WAQE), acetonic (WAE), and alcoholic (WOHE) watercress extracts. The effect of subchronic administration of watercress extracts on oxidative stress was also studied. Materials and Methods: WAQE, WAE, and WOHE were obtained and administered orally. Alloxan (200 mg/kg) and streptozotocin (60 mg/kg) were applied to induce hyperglycemia in male Wistar rats. Phenolic and flavonoid content, as well as antioxidant activity of the extracts were measured. The acute and subchronic effects (8 weeks) of WAQE were evaluated. The activity of antioxidant enzymes levels of malondialdehyde, hepatic enzyme markers in the serum, and renal function markers, were assessed. Histopathological evaluation of the pancreas, kidney, and liver was performed using hematoxylin-eosin staining. Results: Watercress extracts have high concentrations of phenols, polyphenols, and flavonoids, in addition to a very high antioxidant effect. The hypoglycemic effect of WAQE upon acute administration was 76.6% higher than that of insulin. When administered chronically, glucose levels were normalized on the third week up to the eighth week. Furthermore, the antioxidant enzymes and biochemical parameters improved. Conclusion: WAQE administration to diabetic rats reduced oxidative stress damage and decreased glucose levels. This study supports the use of this plant for the treatment of diabetes.


Author(s):  
W. M. Schaffer ◽  
T. V. Bronnikova

Reactive oxygen species (ROS) and peroxidase-oxidase (PO) reactions are Janus-faced contributors to cellular metabolism. At low concentrations, reactive oxygen species serve as signaling molecules; at high concentrations, as destroyers of proteins, lipids and DNA. Correspondingly, PO reactions are both sources and consumers of ROS. In the present paper, we study a well-tested model of the PO reaction based on horseradish peroxidase chemistry. Our principal predictions are these: 1. Under hypoxia, the PO reaction can emit pulses of hydrogen peroxide at apparently arbitrarily long intervals. 2. For a wide range of input rates, continuing infusions of ROS are transduced into bounded dynamics. 3. The response to ROS input is hysteretic. 4. With sufficient input, regulatory capacity is exceeded and hydrogen peroxide, but not superoxide, accumulates. These results are discussed with regard to the episodic nature of neurodevelopmental and neurodegenerative diseases that have been linked to oxidative stress and to downstream interactions that may result in positive feedback and pathology of increasing severity.


2017 ◽  
Vol 37 (suppl_1) ◽  
Author(s):  
Conner C Feldman ◽  
Ting Zhou ◽  
Noel Phan ◽  
Bo Liu

Objectives: Oxidative stress underlies major vascular diseases including atherosclerosis and abdominal aortic aneurysm. Hydrogen peroxide (H2O2) is widely used to trigger oxidative stress in vitro for the study of apoptosis. However, we have previously shown that vascular smooth muscle cells (SMCs) respond to high concentrations (>1 mM) of H2O2 with necrosis. Traditionally regarded as incidental form of cell death, necrosis can occur through different mechanisms mediated by distinct intracellular signaling networks. The precise knowledge of death pathway is essential to the design of therapeutic strategy targeting cell death. The goal of the current study is to determine how H2O2 induces necrosis in SMCs. Methods: Mouse vascular aortic smooth muscle cell line, MOVAS, were treated with 3mM H2O2 for 2 hours, after which cell death was analyzed using flow cytometry and protein expression determined via western blot. Results: SMCs underwent apoptosis and necrosis in response to 0.3 and 3 mM H2O2, respectively. The 3mM H2O2 group died via a caspase-independent mechanism. Expression of common autophagy-associated proteins were unaffected. Additionally, different autophagy activators and inhibitors only moderately facilitated the pro-necrotic effect of H2O2. The H2O2-induced necrosis was not affected by necroptosis inhibitors including necrostatin-1s or by SiRNA silencing of necroptosis mediators RIP1, RIP3 and MLKL. Furthermore, ferroptosis and CypD inhibitors did not provide protection from necrosis induced by H2O2. In contrast, the necrotic response was attenuated by the PARP-1 inhibitor 3-aminobenzamide (37.10±13.72% vs 82.05±0.64%). Moreover, an PARP1 siRNA also reduced necrosis. PARP-1 is the central mediator of a necroptosis mechanism called parthanatos. Conclusions: Our data demonstrates that parthanatos constitutes a major mechanism underlying the necrotic response to high concentrations of H2O2. Current studies delineate the involvement of parthanatos in myocardial ischemia/reperfusion injury, cardiovascular ailments, and atherosclerosis. The present study may provide a new perspective on targeting PARP-1 for the protection of SMCs and likely cardiac myocytes against oxidative stress.


2016 ◽  
Vol 7 (5) ◽  
pp. 2451-2461 ◽  
Author(s):  
Gui-dong Huang ◽  
Xian-feng Zhong ◽  
Ze-yuan Deng ◽  
Rong Zeng

Ginsenoside Re is an active component in ginseng that has attracted much attention because of its evident therapeutic effects on the cardiovascular system.


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