scholarly journals Zanthoxylum heitzii Modulates Ferric Nitrilotriacetate-Dependent Oxidative Alterations in Four Vital Organs: An In Vitro Organoprotective Model

2017 ◽  
Vol 2017 ◽  
pp. 1-11
Author(s):  
Jacques Joël Essogo ◽  
Bruno Moukette Moukette ◽  
Francine Nzufo Tankeu ◽  
Pauline Nanfack ◽  
Constant Anatole Pieme
Keyword(s):  
Oxidative Stress ◽  
Oxidative Damage ◽  
Methanolic Extract ◽  
Ferric Nitrilotriacetate ◽  
Degenerative Disorders ◽  
Reactive Compound ◽  
Liver Homogenates ◽  
The Brain ◽  
Zanthoxylum Heitzii

Ferric nitrilotriacetate (Fe-NTA) is a highly reactive compound used to induce degenerative disorders through oxidative stress (OS). Zanthoxylum heitzii (Z. heitzii) is a spice used as a medicinal plant to treat a variety of illnesses. This study investigated the ability of extracts from the leaves, fruits, roots, and barks of Z. Heitzii to inhibit Fe-NTA mediated oxidative damage in rats. The supernatant of rat liver homogenates was pretreated with the extracts for one hour before the induction of oxidative damage using a solution of Fe-NTA (400 mM). The activities of superoxide dismutase (SOD), catalase, and peroxidases were measured together with the marker of lipid peroxidation and the level of glutathione. The pretreated groups showed a significant increase in the activity of SOD, catalase, and peroxidases. The methanolic extract from the leaves of Z. heitzii (36.78 ± 3.30) and aqueous extract from the fruits (37.01 ± 2.52) showed the highest activities of SOD in the liver. The lowest concentration of MDA was found in the liver, and the glutathione was greater in the brain. Conclusively, these results suggest that Z. heitzii might be a chemoprotector which may be used in for prevention of distinct types of diseases induced by oxidative stress.

scholarly journals Mn Inhibits GSH Synthesis via Downregulation of Neuronal EAAC1 and Astrocytic xCT to Cause Oxidative Damage in the Striatum of Mice

2018 ◽  
Vol 2018 ◽  
pp. 1-15 ◽  
Author(s):  
Xinxin Yang ◽  
Haibo Yang ◽  
Fengdi Wu ◽  
Zhipeng Qi ◽  
Jiashuo Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Oxidative Damage ◽  
Dependent Manner ◽  
Protein Levels ◽  
Key Factor ◽  
Protein Sulfhydryl ◽  
Mrna And Protein Expression ◽  
The Brain

Excessive manganese (Mn) can accumulate in the striatum of the brain following overexposure. Oxidative stress is a well-recognized mechanism in Mn-induced neurotoxicity. It has been proven that glutathione (GSH) depletion is a key factor in oxidative damage during Mn exposure. However, no study has focused on the dysfunction of GSH synthesis-induced oxidative stress in the brain during Mn exposure. The objective of the present study was to explore the mechanism of Mn disruption of GSH synthesis via EAAC1 and xCT in vitro and in vivo. Primary neurons and astrocytes were cultured and treated with different doses of Mn to observe the state of cells and levels of GSH and reactive oxygen species (ROS) and measure mRNA and protein expression of EAAC1 and xCT. Mice were randomly divided into seven groups, which received saline, 12.5, 25, and 50 mg/kg MnCl2, 500 mg/kg AAH (EAAC1 inhibitor) + 50 mg/kg MnCl2, 75 mg/kg SSZ (xCT inhibitor) + 50 mg/kg MnCl2, and 100 mg/kg NAC (GSH rescuer) + 50 mg/kg MnCl2 once daily for two weeks. Then, levels of EAAC1, xCT, ROS, GSH, malondialdehyde (MDA), protein sulfhydryl, carbonyl, 8-hydroxy-2-deoxyguanosine (8-OHdG), and morphological and ultrastructural features in the striatum of mice were measured. Mn reduced protein levels, mRNA expression, and immunofluorescence intensity of EAAC1 and xCT. Mn also decreased the level of GSH, sulfhydryl, and increased ROS, MDA, 8-OHdG, and carbonyl in a dose-dependent manner. Injury-related pathological and ultrastructure changes in the striatum of mice were significantly present. In conclusion, excessive exposure to Mn disrupts GSH synthesis through inhibition of EAAC1 and xCT to trigger oxidative damage in the striatum.

scholarly journals Effect of Shuangdan Mingmu capsule, a Chinese herbal formula, on oxidative stress-induced apoptosis of pericytes through PARP/GAPDH pathway

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Fujiao Nie ◽  
Jiazhao Yan ◽  
Yanjun Ling ◽  
Zhengrong Liu ◽  
Chaojun Fu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Oxidative Damage ◽  
Damage Model ◽  
B Cell Lymphoma ◽  
Cell Counting ◽  
Network Pharmacology ◽  
Diabetic Patients ◽  
Induced Apoptosis

Abstract Background Diabetic retinopathy (DR) has become a worldwide concern because of the rising prevalence rate of diabetes mellitus (DM). Despite much energy has been committed to DR research, it remains a difficulty for diabetic patients all over the world. Since apoptosis of retinal microvascular pericytes (RMPs) is the early characteristic of DR, this study aimed to reveal the mechanism of Shuangdan Mingmu (SDMM) capsule, a Chinese patent medicine, on oxidative stress-induced apoptosis of pericytes implicated with poly (ADP-ribose) polymerase (PARP) / glyceraldehyde 3-phosphate dehydrogenase (GAPDH) pathway. Methods Network pharmacology approach was performed to predict biofunction of components of SDMM capsule dissolved in plasma on DR. Both PARP1 and GAPDH were found involved in the hub network of protein-protein interaction (PPI) of potential targets and were found to take part in many bioprocesses, including responding to the regulation of reactive oxygen species (ROS) metabolic process, apoptotic signaling pathway, and response to oxygen levels through enrichment analysis. Therefore, in vitro research was carried out to validate the prediction. Human RMPs cultured with media containing 0.5 mM hydrogen oxide (H2O2) for 4 h was performed as an oxidative-damage model. Different concentrations of SDMM capsule, PARP1 inhibitor, PARP1 activation, and GAPDH inhibitor were used to intervene the oxidative-damage model with N-Acetyl-L-cysteine (NAC) as a contrast. Flow cytometry was performed to determine the apoptosis rate of cells and the expression of ROS. Cell counting kit 8 (CCK8) was used to determine the activity of pericytes. Moreover, nitric oxide (NO) concentration of cells supernatant and expression of endothelial nitric oxide synthase (eNOS), superoxide dismutase (SOD), B cell lymphoma 2 (BCL2), vascular endothelial growth factor (VEGF), endothelin 1 (ET1), PARP1, and GAPDH were tested through RT-qPCR, western blot (WB), or immunocytochemistry (ICC). Results Overproduction of ROS, high apoptotic rate, and attenuated activity of pericytes were observed after cells were incubated with media containing 0.5 mM H2O2. Moreover, downregulation of SOD, NO, BCL2, and GAPDH, and upregulation of VEGFA, ET1, and PARP1 were discovered after cells were exposed to 0.5 mM H2O2 in this study, which could be improved by PARP1 inhibitor and SDMM capsule in a dose-dependent way, whereas worsened by PARP1 activation and GAPDH inhibitor. Conclusions SDMM capsule may attenuate oxidative stress-induced apoptosis of pericytes through downregulating PARP expression and upregulating GAPDH expression.

scholarly journals Vascular Dysfunction Induced by Mercury Exposure

2019 ◽  
Vol 20 (10) ◽  
pp. 2435 ◽  
Author(s):  
Tetsuya Takahashi ◽  
Takayoshi Shimohata
Keyword(s):  
Oxidative Stress ◽  
Vascular Dysfunction ◽  
Brain Parenchyma ◽  
Transport Systems ◽  
Mehg Exposure ◽  
In Vivo Models ◽  
The Central Nervous System ◽  
The Brain

Methylmercury (MeHg) causes severe damage to the central nervous system, and there is increasing evidence of the association between MeHg exposure and vascular dysfunction, hemorrhage, and edema in the brain, but not in other organs of patients with acute MeHg intoxication. These observations suggest that MeHg possibly causes blood–brain barrier (BBB) damage. MeHg penetrates the BBB into the brain parenchyma via active transport systems, mainly the l-type amino acid transporter 1, on endothelial cell membranes. Recently, exposure to mercury has significantly increased. Numerous reports suggest that long-term low-level MeHg exposure can impair endothelial function and increase the risks of cardiovascular disease. The most widely reported mechanism of MeHg toxicity is oxidative stress and related pathways, such as neuroinflammation. BBB dysfunction has been suggested by both in vitro and in vivo models of MeHg intoxication. Therapy targeted at both maintaining the BBB and suppressing oxidative stress may represent a promising therapeutic strategy for MeHg intoxication. This paper reviews studies on the relationship between MeHg exposure and vascular dysfunction, with a special emphasis on the BBB.

scholarly journals Evaluation of radical scavenging system in amoeba Chaos carolinense during nutrient deprivation

2017 ◽  
Vol 7 (4) ◽  
pp. 20160113 ◽  
Author(s):  
Yuru Deng ◽  
Edlyn Li-Hui Lee ◽  
Ketpin Chong ◽  
Zakaria A. Almsherqi
Keyword(s):  
Oxidative Stress ◽  
Oxidative Damage ◽  
Nucleic Acids ◽  
Cellular Response ◽  
Molecular Mechanisms ◽  
Antioxidant Activities ◽  
Radical Scavenging ◽  
Cellular Responses ◽  
Biological Macromolecules

The frequent appearance of non-lamellar membrane arrangements such as cubic membranes (CMs) in cells under stressed or pathological conditions points to an intrinsic cellular response mechanism. CM represents highly curved, three-dimensional nano-periodic structures that correspond to mathematically well-defined triply periodic minimal surfaces. Specifically, cellular membrane may transform into CM organization in response to pathological, inflammatory and oxidative stress conditions. CM organization, thus, may provide an advantage to cope with various types of stress. The identification of inducible membrane systems, such as in the mitochondrial inner membranes to cubic morphology upon starvation, opens new avenues for understanding the molecular mechanisms of cellular responses to oxidative stress. In this study, we compared the cellular responses of starved and fed amoeba Chaos carolinense to oxidative stress. Food deprivation from C. carolinense induces a significant increase in prooxidants such as superoxide and hydrogen peroxide. Surprisingly, we observed a significant lower rate of biomolecular damage in starved cells (with higher free radicals generation) when compared with fed cells. Specifically, lipid and RNA damages were significantly less in starved cells compared with fed cells. This observation was not due to the upregulation of intracellular antioxidants, as starved amoeba show reduced antioxidant enzymatic activities; however, it could be attributed to CM formation. CM could uptake and retain short segments of nucleic acids (resembles cellular RNA) in vivo and in vitro. Previous results showed that nucleic acids retained within CM sustain a minimal oxidative damage in vitro upon exposure to high level of superoxide. We thus propose that CM may act as a ‘protective’ shelter to minimize the oxidation of biologically essential macromolecules such as RNA. In summary, we examined enzymatic antioxidant activities as well as oxidative damage biomarkers in starved amoeba C. carolinense in correlation with the potential role of CM as an optimal intracellular membrane organization for the protection of biological macromolecules against oxidative damage.

scholarly journals LongShengZhi Capsule Attenuates Alzheimer-Like Pathology in APP/PS1 Double Transgenic Mice by Reducing Neuronal Oxidative Stress and Inflammation

2020 ◽  
Vol 12 ◽  
Author(s):  
Zequn Yin ◽  
Xuerui Wang ◽  
Shihong Zheng ◽  
Peichang Cao ◽  
Yuanli Chen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Transgenic Mice ◽  
Amyloid Β ◽  
B Cell Lymphoma ◽  
Acanthopanax Senticosus ◽  
Neuroprotective Effects ◽  
Long Term Treatment ◽  
Double Transgenic Mice ◽  
The Brain

Alzheimer’s disease (AD) is the most common form of dementia in the elderly. It may be caused by oxidative stress, inflammation, and cerebrovascular dysfunctions in the brain. LongShengZhi Capsule (LSZ), a traditional Chinese medicine, has been approved by the China Food and Drug Administration for treatment of patients with cardiovascular/cerebrovascular disease. LSZ contains several neuroprotective ingredients, including Hirudo, Astmgali Radix, Carthami Flos (Honghua), Persicae Semen (Taoren), Acori Tatarinowii Rhizoma (Shichangpu), and Acanthopanax Senticosus (Ciwujia). In this study, we aimed to determine the effect of LSZ on the AD process. Double transgenic mice expressing the amyloid-β precursor protein and mutant human presenilin 1 (APP/PS1) to model AD were treated with LSZ for 7 months starting at 2 months of age. LSZ significantly improved the cognition of the mice without adverse effects, indicating its high degree of safety and efficacy after a long-term treatment. LSZ reduced AD biomarker Aβ plaque accumulation by inhibiting β-secretase and γ-secretase gene expression. LSZ also reduced p-Tau expression, cell death, and inflammation in the brain. Consistently, in vitro, LSZ ethanol extract enhanced neuronal viability by reducing L-glutamic acid-induced oxidative stress and inflammation in HT-22 cells. LSZ exerted antioxidative effects by enhancing superoxide dismutase and glutathione peroxidase expression, reduced Aβ accumulation by inhibiting β-secretase and γ-secretase mRNA expression, and decreased p-Tau level by inhibiting NF-κB-mediated inflammation. It also demonstrated neuroprotective effects by regulating the Fas cell surface death receptor/B-cell lymphoma 2/p53 pathway. Taken together, our study demonstrates the antioxidative stress, anti-inflammatory, and neuroprotective effects of LSZ in the AD-like pathological process and suggests it could be a potential medicine for AD treatment.

Oxidative stress-related responses of Bifidobacterium longum subsp. longum BBMN68 at the proteomic level after exposure to oxygen

Microbiology ◽  
2011 ◽  
Vol 157 (6) ◽  
pp. 1573-1588 ◽  
Author(s):  
Man Xiao ◽  
Pan Xu ◽  
Jianyun Zhao ◽  
Zeng Wang ◽  
Fanglei Zuo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Oxidative Damage ◽  
Bifidobacterium Longum ◽  
Transcriptional Level ◽  
Low Oxygen ◽  
Oxygen Stress ◽  
Dna Oxidative Damage ◽  
Proteomic Approach ◽  
Protective Proteins

Bifidobacterium longum subsp. longum BBMN68, an anaerobic probiotic isolated from healthy centenarian faeces, shows low oxygen (3 %, v/v) tolerance. To understand the effects of oxidative stress and the mechanisms protecting against it in this strain, a proteomic approach was taken to analyse changes in the cellular protein profiles of BBMN68 under the following oxygen-stress conditions. Mid-exponential phase BBMN68 cells grown in MRS broth at 37 °C were exposed to 3 % O2 for 1 h (I) or 9 h (II), and stationary phase cells were subjected to 3 % O2 for 1 h (III). Respective controls were grown under identical conditions but were not exposed to O2. A total of 51 spots with significant changes after exposure to oxygen were identified, including the oxidative stress-protective proteins alkyl hydroperoxide reductase C22 (AhpC) and pyridine nucleotide-disulfide reductase (PNDR), and the DNA oxidative damage-protective proteins DNA-binding ferritin-like protein (Dps), ribonucleotide reductase (NrdA) and nucleotide triphosphate (NTP) pyrophosphohydrolases (MutT1). Changes in polynucleotide phosphorylase (PNPase) plus enolase, which may play important roles in scavenging oxidatively damaged RNA, were also found. Following validation at the transcriptional level of differentially expressed proteins, the physiological and biochemical functions of BBMN68 Dps were further proven by in vitro and in vivo tests under oxidative stress. Our results reveal the key oxidative stress-protective proteins and DNA oxidative damage-protective proteins involved in the defence strategy of BBMN68 against oxygen, and provide the first proteomic information toward understanding the responses of Bifidobacterium and other anaerobes to oxygen stress.

scholarly journals Lycopene Treatment Ameliorates Amyloid Plaque Deposition and Memory Impairment in the APP/PS1 Mice

2021 ◽  
Author(s):  
Shanshan Ou ◽  
Yinchao Fang ◽  
Tong Wu ◽  
Jie Xu ◽  
Kaihua Guo
Keyword(s):  
Oxidative Stress ◽  
Oxidative Damage ◽  
Western Blot ◽  
Chronic Inflammation ◽  
Signal Pathway ◽  
Qualitative Assessment ◽  
Cell Cytotoxicity ◽  
Rt Pcr

Abstract Alzheimer’s disease (AD) is a neurodegenerative condition associated with oxidative stress and neuroinflammation. Lycopene has previously been shown to ameliorate neuroinflammation and exert protection against oxidative damage in neuroblastoma cells. The role of this compound in reversing cognitive dysfunction in AD has yet to be determined. The present study investigates the role of lycopene in AD with an in vitro Aβ1-42-induced cell cytotoxicity model as well as the in vivo APP/PS1 mouse model. The activation of Nrf2 signal pathway was assessed using western blot and RT-PCR. MDA, 8-OHdG, ROS, SOD, GHS and GSSG measurements were carried out using the specialized assay kits. The Morris water maze was used to examine qualitative assessment of memory and spatial learning. Immunofluorescence was used to visualize astrocytes and microglia activation as well as brain β-amyloid (Aβ) deposition. The NeuN positive cells were detected by immunofluorescence and western blot. Levels of cerebral cytokines were quantified using RT-PCR. Lycopene ameliorates oxidative damage in the Aβ1-42-triggered cell cytotoxicity model via Nrf2-ARE signal pathway activation, which is regulated by AKT-GSK3β pathway. In addition, lycopene improves the cognitive impairment and reduces the Aβ deposition. Mechanistically, lycopene attenuates neuron loss, decreases chronic inflammation and activates cerebral Nrf2-ARE signaling pathway in APP/PS1 mice. The results suggest that lycopene alleviates oxidative stress via AKT- Nrf2-ARE pathway. And early administration of lycopene improves cognitive deficits by reducing Aβ deposition, neuronal loss and decreasing the degree of chronic inflammation.

scholarly journals Curcumin Reduce Sodium Fluoride-Induced Oxidative Stress in Rat Brain

2018 ◽  
Vol 15 (1) ◽  
pp. 71-77 ◽  
Author(s):  
Nagapuri Kiran Kumar ◽  
Mesram Nageshwar ◽  
Karnati Pratap Reddy
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Oxidative Damage ◽  
Oral Administration ◽  
Rat Brain ◽  
Sodium Fluoride ◽  
Oxidative Stress Markers ◽  
Stress Markers ◽  
The Brain

This study reports the ameliorative role of curcumin against sodium fluoride (NaF) induced oxidative stress in the brain of rats. The rats were divided into control, NaF (20 mg/kg), NaF+Curcumin (20mg/kg) and Curcumin (20mg/kg) groups respectively and treated at everyday interval for 60 consecutive days. Oxidative stress markers in the brain were measured at 60th day. NaF treatment significantly increased LPO content, but decreased the level of GSH and activities of SOD, GPx, and CAT the brain of rats in comparison to the control rats. Oral administration of curcumin to fluoride exposed rats significantly reversed the content of lipid peroxidation, as well as enhanced the level of GSH and SOD, GPx and CAT activities to normal compared to NaF exposed rats. Thus, curcumin showed the potential to prevent sodium fluoride induced oxidative damage in the brain of rats and curcumin may be useful agents against neurodegeneration in the brain.

scholarly journals Age-dependent effect of oxidative stress on cardiac sarcoplasmic reticulum vesicles

2008 ◽  
pp. S49-S54
Author(s):  
E Babušíková ◽  
M Jeseňák ◽  
D Dobrota ◽  
N Tribulová ◽  
P Kaplán
Keyword(s):  
Oxidative Stress ◽  
Sarcoplasmic Reticulum ◽  
Oxidative Damage ◽  
Structural Changes ◽  
Membrane Surface ◽  
Thiobarbituric Acid ◽  
Surface Hydrophobicity ◽  
Cardiac Sarcoplasmic Reticulum ◽  
Age Related

The oxidative stress hypothesis of aging suggests that accumulation of oxidative damage is a key factor of the alterations in physiological function during aging. We studied age-related sensitivity to oxidative modifications of proteins and lipids of cardiac sarcoplasmic reticulum (SR) isolated from 6-, 15- and 26-month-old rats. Oxidative stress was generated in vitro by exposing SR vesicles to 0.1 mmol/l FeSO4/EDTA + 1 mmol/l H2O2 at 37 degrees C for 60 min. In all groups, oxidative stress was associated with decreased membrane surface hydrophobicity, as detected by 1-anilino-8-naphthalenesulfonate as a probe. Structural changes in SR membranes were accompanied by degradation of tryptophan and significant accumulation of protein dityrosines, protein conjugates with lipid peroxidation products, conjugated dienes and thiobarbituric acid reactive substances. The sensitivity to oxidative damage was most pronounced in SR of 26-month-old rat. Our results indicate that aging and oxidative stress are associated with accumulation of oxidatively damaged proteins and lipids and these changes could contribute to cardiovascular injury.

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