Hydrogen peroxide regulates the cholinergic signal in a concentration dependent manner

Life Sciences ◽  
2007 ◽  
Vol 80 (24-25) ◽  
pp. 2221-2226 ◽  
Author(s):  
Karin U. Schallreuter ◽  
Souna Elwary
2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Foncham Evans Ngwenah ◽  
Kada Sanda Antoine ◽  
Salah Martin ◽  
Tume Christopher ◽  
Oumar Mahamat

Background. Natural products have been said to show immunomodulatory and antioxidant activities. The research study was aimed to assess the immunomodulatory and free radical scavenging activities of crude polysaccharide from dry mushroom fruiting bodies of Termitomyces le-testui. Materials and Methods. Hot water extract of polysaccharide extract of T. le-testui was prepared and tested in white albino Wister rats for its immunomodulatory activities effect on methylprednisolone-immunosuppressed animals. In addition, the radical scavenging activity of the polysaccharide was evaluated using nitrite and hydrogen peroxide. Results. The result of the study showed that the polysaccharide T. le-testui increases the phagocytic index, energy metabolism of macrophages, spleen index, and nitric oxide in a concentration-dependent manner in immunosuppressed animals. Also, it was observed that the extract increased dose-dependent total oxidative stress and thymus index. Finally, the crude polysaccharide-rich extract showed nitrite and hydrogen peroxide scavenging activity in a concentration-dependent manner. Conclusion. Polysaccharide-rich extract possesses immunomodulatory and antioxidant properties.


2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Hui Zhou ◽  
Baocai Fu ◽  
Bo Xu ◽  
Xiangquan Mi ◽  
Gang Li ◽  
...  

Endothelial dysfunction is the key player in the development and progression of vascular events. Oxidative stress is involved in endothelial injury. Rosmarinic acid (RA) is a natural polyphenol with antioxidative, antiapoptotic, and anti-inflammatory properties. The present study investigates the protective effect of RA on endothelial dysfunction induced by hydrogen peroxide (H2O2). Compared with endothelium-denuded aortic rings, the endothelium significantly alleviated the decrease of vasoconstrictive reactivity to PE and KCl induced by H2O2. H2O2 pretreatment significantly injured the vasodilative reactivity to ACh in endothelium-intact aortic rings in a concentration-dependent manner. RA individual pretreatment had no obvious effect on the vasoconstrictive reaction to PE and KCl, while its cotreatment obviously mitigated the endothelium-dependent relaxation impairments and the oxidative stress induced by H2O2. The RA cotreatment reversed the downregulation of AMPK and eNOS phosphorylation induced by H2O2 in HAEC cells. The pretreatment with the inhibitors of AMPK (compound C) and eNOS (L-NAME) wiped off RA’s beneficial effects. All these results demonstrated that RA attenuated the endothelial dysfunction induced by oxidative stress by activating the AMPK/eNOS pathway.


2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Ruslana Vasylkovska ◽  
Natalia Petriv ◽  
Halyna Semchyshyn

Hormesis is a phenomenon of particular interest in biology, medicine, pharmacology, and toxicology. In this study, we investigated the relationship between H2O2-induced hormetic response inS. cerevisiaeand carbon sources in yeast growth medium. In general, our data indicate that (i) hydrogen peroxide induces hormesis in a concentration-dependent manner; (ii) the effect of hydrogen peroxide on yeast reproductive ability depends on the type of carbon substrate in growth medium; and (iii) metabolic and growth rates as well as catalase activity play an important role in H2O2-induced hormetic response in yeast.


2021 ◽  
Vol 18 (10) ◽  
pp. 2109-2115
Author(s):  
Waqas Ahmad Shams ◽  
Gauhar Rehman ◽  
Samuel Okwudili Onoja ◽  
Abid Ali ◽  
Khurshaid Khan ◽  
...  

Purpose: To evaluate the in vitro antidiabetic, anti-inflammatory and antioxidant potential of the ethanol extract of Uromastyx hardwickii Skin (UHSEE). Methods: The in vitro effects of UHSEE at various concentrations (10 - 250 µg/mL) on the activities of ߙ-amylase, ߙ-glucosidase and glucose uptake by yeast cells were used to evaluate its antidiabetic potential. Nitric oxide (NO), 2,2-diphenyl-1-picrylhydrazyl (DPPH) and hydrogen peroxide inhibitory assay were employed to determine its antioxidant effects, while the anti-inflammatory effects were evaluated using human red blood cell (HRBC) membrane stabilization assay. Results: UHSEE inhibited ߙ-amylase and ߙ-glucosidase enzymes but increased glucose uptake by yeast cells in a concentration-dependent manner (p < 0.05). It also inhibited NO, DPPH, hydrogen peroxide and HRBC hemolysis in a concentration-dependent manner (p < 0.05). Conclusion: Uromastyx hardwickii skin exhibits promising good antidiabetic, antioxidant and antiinflammatory properties in vitro. However, its true potentials in this regard needs to be evaluted in vivo.


2007 ◽  
Vol 292 (3) ◽  
pp. H1404-H1411 ◽  
Author(s):  
Paul A. Rogers ◽  
William M. Chilian ◽  
Ian N. Bratz ◽  
Robert M. Bryan ◽  
Gregory M. Dick

Previously, we demonstrated that coronary vasodilation in response to hydrogen peroxide (H2O2) is attenuated by 4-aminopyridine (4-AP), an inhibitor of voltage-gated K+ (KV) channels. Using whole cell patch-clamp techniques, we tested the hypothesis that H2O2 increases K+ current in coronary artery smooth muscle cells. H2O2 increased K+ current in a concentration-dependent manner (increases of 14 ± 3 and 43 ± 4% at 0 mV with 1 and 10 mM H2O2, respectively). H2O2 increased a conductance that was half-activated at −18 ± 1 mV and half-inactivated at −36 ± 2 mV. H2O2 increased current amplitude; however, the voltages of half activation and inactivation were not altered. Dithiothreitol, a thiol reductant, reversed the effect of H2O2 on K+ current and significantly shifted the voltage of half-activation to −10 ± 1 mV. N-ethylmaleimide, a thiol-alkylating agent, blocked the effect of H2O2 to increase K+ current. Neither tetraethylammonium (1 mM) nor iberiotoxin (100 nM), antagonists of Ca2+-activated K+ channels, blocked the effect of H2O2 to increase K+ current. In contrast, 3 mM 4-AP completely blocked the effect of H2O2 to increase K+ current. These findings lead us to conclude that H2O2 increases the activity of 4-AP-sensitive KV channels. Furthermore, our data support the idea that 4-AP-sensitive KV channels are redox sensitive and contribute to H2O2-induced coronary vasodilation.


2019 ◽  
Vol 20 (11) ◽  
pp. 2680 ◽  
Author(s):  
Xia Zhao ◽  
Jiankang Fang ◽  
Shuai Li ◽  
Uma Gaur ◽  
Xingan Xing ◽  
...  

Oxidative stress is believed to be one of the main causes of neurodegenerative diseases such as Alzheimer’s disease (AD). The pathogenesis of AD is still not elucidated clearly but oxidative stress is one of the key hypotheses. Here, we found that artemisinin, an anti-malarial Chinese medicine, possesses neuroprotective effects. However, the antioxidative effects of artemisinin remain to be explored. In this study, we found that artemisinin rescued SH-SY5Y and hippocampal neuronal cells from hydrogen peroxide (H2O2)-induced cell death at clinically relevant doses in a concentration-dependent manner. Further studies showed that artemisinin significantly restored the nuclear morphology, improved the abnormal changes in intracellular reactive oxygen species (ROS), reduced the mitochondrial membrane potential, and caspase-3 activation, thereby attenuating apoptosis. Artemisinin also stimulated the phosphorylation of the adenosine monophosphate -activated protein kinase (AMPK) pathway in SH-SY5Y cells in a time- and concentration-dependent manner. Inhibition of the AMPK pathway attenuated the protective effect of artemisinin. These data put together suggested that artemisinin has the potential to protect neuronal cells. Similar results were obtained in primary cultured hippocampal neurons. Cumulatively, these results indicated that artemisinin protected neuronal cells from oxidative damage, at least in part through the activation of AMPK. Our findings support the role of artemisinin as a potential therapeutic agent for neurodegenerative diseases.


Author(s):  
Paula M. Kustiawan ◽  
Hiroyuki Okuyoshi ◽  
Yoshiki Kuse ◽  
Hiroshi Izawa ◽  
Yuichi Saito ◽  
...  

The pharmacological and biological activities of Indonesian propolis are mostly unexplored except for its anticancer properties. This study was designed to explore the protective effects of the methanol extract of Indonesian propolis (MEP) obtained from the stingless bee (Trigona incisa) against light-induced retinal photoreceptor damage. Murine photoreceptor (661W) cells were cultured and treated with MEP. The cells were exposed to cellular stress inducers such as tunicamycin, hydrogen peroxide, and light irradiation. The protective effects of MEP were assessed by determining production of intracellular reactive oxygen species (ROS), analyzing changes in nuclear factor-kappa B (NF-κB) level, analyzing caspase-3/7 activation, and by using the zebrafish retinal degeneration model. MEP significantly reduced cell death induced by tunicamycin, hydrogen peroxide, and white light irradiation in a concentration-dependent manner. The phosphorylation of NF-κB decreased and light-induced activation of caspase-3/7 and intracellular accumulation of ROS were inhibited. The thickness of outer nuclear layer (ONL) in zebrafish retina significantly increased following MEP treatment. The MEP obtained from stingless bee propolis has a protective effect on photoreceptor retinal cells and has the potential to be developed as a supplement in prevention of retinal diseases.


1992 ◽  
Vol 263 (5) ◽  
pp. H1546-H1553
Author(s):  
J. L. Wallace ◽  
K. P. Rioux ◽  
W. McKnight ◽  
L. Carter ◽  
D. Jourd'heuil ◽  
...  

Hemoproteins have been suggested to contribute to various forms of tissue injury by catalyzing the peroxidation of lipids. In this study, the ability of hemoglobin to catalyze the production of a neutrophil-activating factor from arachidonic acid was examined. Incubation of arachidonic acid, hydrogen peroxide, and hemoglobin at 37 degrees C for 30 min resulted in the production of a lipid-extractable substance that was chemotactic for neutrophils in vitro and could stimulate leukocyte adherence in vivo. These actions could be inhibited by two leukotriene B4 (LTB4) receptor antagonists. The peroxidation product cross-reacted significantly with an antibody directed against LTB4, but not with an antibody directed against LTC4. The production of this factor was hemoprotein dependent. Immunoreactive LTB4 and biological activity were produced only when hemoglobin, or another hemoprotein, cytochrome c, was present in the reaction mixture. The amount of the factor produced could be increased in a concentration-dependent manner by increasing the amounts of arachidonic acid or hydrogen peroxide in the reaction mixture. The production of this factor could be inhibited by 5-aminosalicylic acid, catalase, or deferoxamine. Separation of the lipid-extractable products of the peroxidation of arachidonic acid on high-performance liquid chromatography revealed that the immunoreactive (with anti-LTB4) and chemotactic substance had a retention time distinct from that of LTB4 and the hydroxyeicosatetraenoic acids. A lipid-extractable substance with significant cross-reactivity to anti-LTB4 could also be produced if plasma was substituted for arachidonic acid in the reaction mixture.(ABSTRACT TRUNCATED AT 250 WORDS)


2014 ◽  
Vol 84 (1-2) ◽  
pp. 79-91 ◽  
Author(s):  
Amin F. Majdalawieh ◽  
Hyo-Sung Ro

Background: Foam cell formation resulting from disrupted macrophage cholesterol efflux, which is triggered by PPARγ1 and LXRα, is a hallmark of atherosclerosis. Sesamin and sesame oil exert anti-atherogenic effects in vivo. However, the exact molecular mechanisms underlying such effects are not fully understood. Aim: This study examines the potential effects of sesamin (0, 25, 50, 75, 100 μM) on PPARγ1 and LXRα expression and transcriptional activity as well as macrophage cholesterol efflux. Methods: PPARγ1 and LXRα expression and transcriptional activity are assessed by luciferase reporter assays. Macrophage cholesterol efflux is evaluated by ApoAI-specific cholesterol efflux assays. Results: The 50 μM, 75 μM, and 100 μM concentrations of sesamin up-regulated the expression of PPARγ1 (p< 0.001, p < 0.001, p < 0.001, respectively) and LXRα (p = 0.002, p < 0.001, p < 0.001, respectively) in a concentration-dependent manner. Moreover, 75 μM and 100 μM concentrations of sesamin led to 5.2-fold (p < 0.001) and 6.0-fold (p<0.001) increases in PPAR transcriptional activity and 3.9-fold (p< 0.001) and 4.2-fold (p < 0.001) increases in LXR transcriptional activity, respectively, in a concentration- and time-dependent manner via MAPK signaling. Consistently, 50 μM, 75 μM, and 100 μM concentrations of sesamin improved macrophage cholesterol efflux by 2.7-fold (p < 0.001), 4.2-fold (p < 0.001), and 4.2-fold (p < 0.001), respectively, via MAPK signaling. Conclusion: Our findings shed light on the molecular mechanism(s) underlying sesamin’s anti-atherogenic effects, which seem to be due, at least in part, to its ability to up-regulate PPARγ1 and LXRα expression and transcriptional activity, improving macrophage cholesterol efflux. We anticipate that sesamin may be used as a therapeutic agent for treating atherosclerosis.


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