Partially Hydrolyzed Guar Gum Attenuates d-Galactose-Induced Oxidative Stress and Restores Gut Microbiota in Rats

Partially hydrolyzed guar gum (PHGG) has received considerable attention for its various bioactive functions. The injection of d-galactose can cause aging-related injury which is usually resulted from oxidative stress on tissues and cells. In this study, d-galactose (200 mg/kg/day) was injected into rats, and the protective effects of PHGG (500, 1000, and 1500 mg/kg/day) against oxidative damages, as well as its probiotic functions, were analyzed. The results showed that PHGG treatment at a concentration of 1500 mg/kg/day greatly reduced the levels of lactic acid, nitric oxide, inducible nitric oxide synthase, advanced glycation end products, and increased the telomerase activity, by 7.60%, 9.25%, 12.28%, 14.58%, and 9.01%, respectively. Moreover, PHGG significantly elevated the activities of antioxidant enzymes and decreased the content of malondialdehyde in rat serum and brain. The oxidative damage was also significantly alleviated in the liver and hippocampus and the expressions of brain-derived neurotrophic factor and choline acetyltransferase also increased. Furthermore, PHGG treatment could significantly regulated the expression of sirtuin 1, forkhead box O1, and tumor protein p53 in the hippocampus. It also increased the levels of organic acids and improved the composition of intestinal microbiota. These findings demonstrated that PHGG treatment could effectively alleviate the oxidative damage and dysbacteriosis.

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

BMC Complementary Medicine and Therapies ◽

10.1186/s12906-021-03238-w ◽

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.

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Ethanol Extract of Maclura tricuspidata Fruit Protects SH-SY5Y Neuroblastoma Cells against H2O2-Induced Oxidative Damage via Inhibiting MAPK and NF-κB Signaling

International Journal of Molecular Sciences ◽

10.3390/ijms22136946 ◽

2021 ◽

Vol 22 (13) ◽

pp. 6946

Author(s):

Weishun Tian ◽

Suyoung Heo ◽

Dae-Woon Kim ◽

In-Shik Kim ◽

Dongchoon Ahn ◽

...

Keyword(s):

Oxidative Stress ◽

Free Radical ◽

Oxidative Damage ◽

Cell Damage ◽

Antioxidant Properties ◽

Radical Scavenging ◽

Biologically Active ◽

Mitogen Activated Protein Kinase ◽

Protective Effects ◽

Neuroprotective Effects

Free radical generation and oxidative stress push forward an immense influence on the pathogenesis of neurodegenerative diseases such as Alzheimer’s disease and Parkinson’s disease. Maclura tricuspidata fruit (MT) contains many biologically active substances, including compounds with antioxidant properties. The current study aimed to investigate the neuroprotective effects of MT fruit on hydrogen peroxide (H2O2)-induced neurotoxicity in SH-SY5Y cells. SH-SY5Y cells were pretreated with MT, and cell damage was induced by H2O2. First, the chemical composition and free radical scavenging properties of MT were analyzed. MT attenuated oxidative stress-induced damage in cells based on the assessment of cell viability. The H2O2-induced toxicity caused by ROS production and lactate dehydrogenase (LDH) release was ameliorated by MT pretreatment. MT also promoted an increase in the expression of genes encoding the antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT). MT pretreatment was associated with an increase in the expression of neuronal genes downregulated by H2O2. Mechanistically, MT dramatically suppressed H2O2-induced Bcl-2 downregulation, Bax upregulation, apoptotic factor caspase-3 activation, Mitogen-activated protein kinase (MAPK) (JNK, ERK, and p38), and Nuclear factor-κB (NF-κB) activation, thereby preventing H2O2-induced neurotoxicity. These results indicate that MT has protective effects against H2O2-induced oxidative damage in SH-SY5Y cells and can be used to prevent and protect against neurodegeneration.

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Role of Oxidative and Nitro-Oxidative Damage in Silver Nanoparticles Cytotoxic Effect against Human Pancreatic Ductal Adenocarcinoma Cells

Oxidative Medicine and Cellular Longevity ◽

10.1155/2018/8251961 ◽

2018 ◽

Vol 2018 ◽

pp. 1-15 ◽

Cited By ~ 17

Author(s):

Ewelina Barcińska ◽

Justyna Wierzbicka ◽

Agata Zauszkiewicz-Pawlak ◽

Dagmara Jacewicz ◽

Aleksandra Dabrowska ◽

...

Keyword(s):

Oxidative Stress ◽

Nitric Oxide ◽

Pancreatic Cancer ◽

Silver Nanoparticles ◽

Oxidative Damage ◽

Pancreatic Ductal Adenocarcinoma ◽

Cytotoxic Effect ◽

Mrna Level ◽

Ductal Adenocarcinoma ◽

Adenocarcinoma Cells

Pancreatic ductal adenocarcinoma is one of the most aggressive human malignancies, where the 5-year survival rate is less than 4% worldwide. Successful treatment of pancreatic cancer is a challenge for today’s oncology. Several studies showed that increased levels of oxidative stress may cause cancer cells damage and death. Therefore, we hypothesized that oxidative as well as nitro-oxidative stress is one of the mechanisms inducing pancreatic cancer programmed cell death. We decided to use silver nanoparticles (AgNPs) (2.6 and 18 nm) as a key factor triggering the reactive oxygen species (ROS) and reactive nitrogen species (RNS) in pancreatic ductal adenocarcinoma cells (PANC-1). Previously, we have found that AgNPs induced PANC-1 cells death. Furthermore, it is known that AgNPs may induce an accumulation of ROS and alteration of antioxidant systems in different type of tumors, and they are indicated as promising agents for cancer therapy. Then, the aim of our study was to evaluate the implication of oxidative and nitro-oxidative stress in this cytotoxic effect of AgNPs against PANC-1 cells. We determined AgNP-induced increase of ROS level in PANC-1 cells and pancreatic noncancer cell (hTERT-HPNE) for comparison purposes. We found that the increase was lower in noncancer cells. Reduction of mitochondrial membrane potential and changes in the cell cycle were also observed. Additionally, we determined the increase in RNS level: nitric oxide (NO) and nitric dioxide (NO2) in PANC-1 cells, together with increase in family of nitric oxide synthases (iNOS, eNOS, and nNOS) at protein and mRNA level. Disturbance of antioxidant enzymes: superoxide dismutase (SOD1, SOD2, and SOD3), glutathione peroxidase (GPX-4) and catalase (CAT) were proved at protein and mRNA level. Moreover, we showed cells ultrastructural changes, characteristic for oxidative damage. Summarizing, oxidative and nitro-oxidative stress and mitochondrial disruption are implicated in AgNPs-mediated death in human pancreatic ductal adenocarcinoma cells.

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Four Novel Dammarane-Type Triterpenoids from Pearl Knots of Panax ginseng Meyer cv. Silvatica

Molecules ◽

10.3390/molecules24061159 ◽

2019 ◽

Vol 24 (6) ◽

pp. 1159 ◽

Cited By ~ 1

Author(s):

Zeng Qi ◽

Zhuo Li ◽

Xuewa Guan ◽

Cuizhu Wang ◽

Fang Wang ◽

...

Keyword(s):

Oxidative Stress ◽

Inflammatory Response ◽

Oxidative Damage ◽

Cigarette Smoke ◽

Panax Ginseng ◽

Inflammatory Reaction ◽

A549 Cells ◽

Protective Effects

Panax ginseng Meyer cv. Silvatica (PGS), which is also known as “Lin-Xia-Shan-Shen” or “Zi-Hai” in China, is grown in forests and mountains by broadcasting the seeds of ginseng and is harvested at the cultivation age of 15–20 years. In this study, four new dammarane-type triterpenoids, ginsengenin-S1 (1), ginsengenin-S2 (2), ginsenoside-S3 (3), ginsenoside-S4 (4), along with one known compound were isolated from pearl knots of PGS. Ginsengenin-S2 significantly alleviated oxidative damage when A549 cells were exposed to cigarette smoke (CS) extract. In addition, ginsengenin-S2 could inhibit the CS-induced inflammatory reaction in A549 cells. Protective effects of ginsengenin-S2 against CS-mediated oxidative stress and the inflammatory response in A549 cells may involve the Nrf2 and HDAC2 pathways.

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Protective effects of a cocktail of lactic acid bacteria on microcystin-LR-induced hepatotoxicity and oxidative damage in BALB/c mice

RSC Advances ◽

10.1039/c7ra03035e ◽

2017 ◽

Vol 7 (33) ◽

pp. 20480-20487 ◽

Cited By ~ 1

Author(s):

Jichun Zhao ◽

Fengwei Tian ◽

Qixiao Zhai ◽

Ruipeng Yu ◽

Hao Zhang ◽

...

Keyword(s):

Oxidative Stress ◽

Lactic Acid ◽

Lactic Acid Bacteria ◽

Oxidative Damage ◽

Protective Effects ◽

And Oxidative Stress

The aim of this study was to investigate the effects of mixed lactic acid bacteria (LAB) against microcystin-LR-exposed hepatotoxicity and oxidative stress in BALB/c mice.

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Melatonin reduces oxidative damage in mouse granulosa cells via restraining JNK-dependent autophagy

Reproduction ◽

10.1530/rep-18-0002 ◽

2018 ◽

Vol 155 (3) ◽

pp. 307-319 ◽

Cited By ~ 7

Author(s):

Yan Cao ◽

Ming Shen ◽

Yi Jiang ◽

Shao-chen Sun ◽

Honglin Liu

Keyword(s):

Oxidative Stress ◽

Oxidative Damage ◽

Mammalian Cells ◽

Therapeutic Strategies ◽

Oxygen Species ◽

Protective Effects ◽

Follicular Atresia ◽

Direct Role ◽

Jnk Pathway

Oxidative stress-induced granulosa cell (GCs) injury is believed to be a common trigger for follicular atresia. Emerging evidence indicates that excessive autophagy occurs in mammalian cells with oxidative damage. N-acetyl-5-methoxytrypamine (melatonin) has been shown to prevent GCs from oxidative injury, although the exact mechanism remains to be elucidated. Here, we first demonstrated that the suppression of autophagy through the JNK/BCL-2/BECN1 signaling is engaged in melatonin-mediated GCs protection against oxidative damage. Melatonin inhibited the loss of GCs viability, formation of GFP-MAP1LC3B puncta, accumulation of MAP1LC3B-II blots, degradation of SQSTM1 and the expression of BECN1, which was correlated with impaired activation of JNK during oxidative stress. On the other hand, blocking of autophagy and/or JNK also reduced the level of H2O2-induced GCs death, but failed to further restore GCs viability in the presence of melatonin. Particularly, the suppression of autophagy provided no additional protective effects when GCs were pretreated with JNK inhibitor and/or melatonin. Importantly, we found that the enhanced interaction between BCL-2 and BECN1 might be a responsive mechanism for autophagy suppression via the melatonin/JNK pathway. Moreover, blocking the downstream antioxidant system of melatonin using specific inhibitors further confirmed a direct role of melatonin/JNK/autophagy axis in preserving GCs survival without scavenging reactive oxygen species (ROS). Taken together, our findings uncover a novel function of melatonin in preventing GCs from oxidative damage by targeting JNK-mediated autophagy, which might contribute to develop therapeutic strategies for patients with ovulation failure-related disorders.

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Antioxidant Effects of Oleuropein on Hydrogen Peroxide-Induced Neuronal Stress- An In Vitro Study

Anti-Inflammatory & Anti-Allergy Agents in Medicinal Chemistry ◽

10.2174/1871523018666190201145824 ◽

2020 ◽

Vol 19 (1) ◽

pp. 74-84 ◽

Cited By ~ 1

Author(s):

Altug Kucukgul ◽

Mehmet M. Isgor ◽

Vesile Duzguner ◽

Meryem N. Atabay ◽

Azime Kucukgul

Keyword(s):

Oxidative Stress ◽

Nitric Oxide ◽

Antioxidant Capacity ◽

Total Antioxidant Capacity ◽

Protective Effects ◽

Glioblastoma Cells ◽

Human Glioblastoma ◽

Antioxidative Properties ◽

Total Antioxidant ◽

Human Glioblastoma Cells

Background: Persistent oxidative stress can lead to chronic inflammation and mediate most chronic diseases including neurological disorders. Oleuropein has been shown to be a potent antioxidant molecule in olive oil leaf having antioxidative properties. Objective: The aim of this study was to investigate the protective effects of oleuropein against oxidative stress in human glioblastoma cells. Methods: Human glioblastoma cells (U87) were pretreated with oleuropein (OP) essential oil 10 µM. After 30 minutes, 100 µM H2O2 was added to the cells for three hours. Cell survival was quantified by colorimetric MTT assay. Glutathione level, total oxidant capacity, total antioxidant capacity and nitric oxide levels were determined by using specific spectrophotometric methods. The relative gene expression level of iNOS was performed by qRT-PCR method. Results: According to viability results, the effective concentration of H2O2 (100µM) significantly decreased cell viability and oleuropein pretreatment significantly prevented the cell losses. Oleuropein regenerated total antioxidant capacity and glutathione levels decreased by H2O2 exposure. In addition, nitric oxide and total oxidant capacity levels were also decreased after administration of oleuropein in treated cells. Conclusion: Oleuropein was found to have potent antioxidative properties in human glioblastoma cells. However, further studies and validations are needed in order to understand the exact neuroprotective mechanism of oleuropein.

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Lipoic acid antagonizes paraquat-induced vascular endothelial dysfunction by suppressing mitochondrial reactive oxidative stress

Toxicology Research ◽

10.1039/c9tx00186g ◽

2019 ◽

Vol 8 (6) ◽

pp. 918-927 ◽

Cited By ~ 5

Author(s):

Li Pang ◽

Ping Deng ◽

Yi-dan Liang ◽

Jing-yu Qian ◽

Li-Chuan Wu ◽

...

Keyword(s):

Oxidative Stress ◽

Nitric Oxide ◽

Endothelial Cells ◽

Endothelial Dysfunction ◽

Lipoic Acid ◽

Microvascular Endothelial Cells ◽

Ros Generation ◽

Protective Effects ◽

Migration Ability ◽

Microvascular Endothelial

Abstract Paraquat (PQ) is a widely used herbicide in the agricultural field. The lack of an effective antidote is the significant cause of high mortality in PQ poisoning. Here, we investigate the antagonistic effects of alpha lipoic acid (α-LA), a naturally existing antioxidant, on PQ toxicity in human microvascular endothelial cells (HMEC-1). All the doses of 250, 500 and 1000 μM α-LA significantly inhibited 1000 μM PQ-induced cytotoxicity in HMEC-1 cells. α-LA pretreatment remarkably diminished the damage to cell migration ability, recovered the declined levels of the vasodilator factor nitric oxide (NO), elevated the expression level of endothelial nitric oxide synthases (eNOS), and inhibited the upregulated expression of vasoconstrictor factor endothelin-1 (ET-1). Moreover, α-LA pretreatment inhibited reactive oxygen species (ROS) generation, suppressed the damage to the mitochondrial membrane potential (ΔΨm) and mitigated the inhibition of adenosine triphosphate (ATP) production in HMEC-1 cells. These results suggested that α-LA could alleviate PQ-induced endothelial dysfunction by suppressing oxidative stress. In summary, our present study provides novel insight into the protective effects and pharmacological potential of α-LA against PQ toxicity in microvascular endothelial cells.

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Nitric Oxide Alleviates Iron Toxicity by Reducing Oxidative Damage and Growth Inhibition in Wheat (Triticum aestivum L.) Seedlings

International Journal of Plant and Environment ◽

10.18811/ijpen.v5i01.3 ◽

2019 ◽

Vol 5 (01) ◽

pp. 16-22

Author(s):

Nalini Pandey ◽

Laxmi Verma

Keyword(s):

Oxidative Stress ◽

Nitric Oxide ◽

Oxidative Damage ◽

Sodium Nitroprusside ◽

Dry Weight ◽

Triticum Aestivum L ◽

Tolerance Index ◽

Promoting Effect ◽

Wheat Seedlings ◽

Protein Thiols

Nitric oxide (NO) is an important bioactive signaling molecule in plants which modulates a variety of physiological processes and responses to abiotic and biotic stresses. In this study, the effects of exogenous NO supplied as sodium nitroprusside (SNP) in wheat seedlings under ironinduced oxidative damage was investigated. An appropriate concentration of NO was determined by conducting a preliminary experiment. In solution culture, wheat seeds were grown in the control (100 μM Fe), and toxic Fe (400 μM Fe) levels and the toxic Fe supply was treated with various levels of (50, 100, 200 and 500 μM) sodium nitroprusside (SNP). The results indicated that 400 μM Fe significantly decreased percentage germination, tolerance index, root lengths as well as fresh and dry weight compared to control. Exogenous SNP attenuated the inhibition of wheat seed germination. The promoting effect was most pronounced at 100 μM SNP. The accumulated concentration of iron and active Fe was significantly decreased by SNP treated Fe toxic seedlings. Toxicity of Fe caused oxidative stress by elevating hydrogen peroxide (H2O2), malondialdehyde (MDA) and proline contents in roots of wheat seedlings. One hundred μM SNP counteracted Fe toxicity by reducing the H2O2, MDA and proline contents of toxic Fe exposed seedlings. Meanwhile, application of SNP markedly reduced the activities of superoxide dismutases (SOD), catalases (CAT), peroxidase (POD), ascorbate peroxidases (APX), non protein thiols (NPT) and of glutathione reductase (GR) and increased ascorbate (ASc) compared with Fe toxic treatment alone, thereby indicating the modulation of the antioxidative capacity in the root under Fe stress by NO. The results indicated that the exogenous application of SNP, improved the antioxidant enzymes activity of wheat seedlings against Fe induced oxidative stress.

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Differential Telomere Shortening in Blood versus Arteries in an Animal Model of Type 2 Diabetes

Journal of Diabetes Research ◽

10.1155/2015/153829 ◽

2015 ◽

Vol 2015 ◽

pp. 1-9 ◽

Cited By ~ 4

Author(s):

Samira Tajbakhsh ◽

Kamelya Aliakbari ◽

Damian J. Hussey ◽

Karen M. Lower ◽

Anthony J. Donato ◽

...

Keyword(s):

Oxidative Stress ◽

Nitric Oxide ◽

Type 2 Diabetes ◽

Vascular Dysfunction ◽

Vascular Complications ◽

Sirtuin 1 ◽

Telomere Shortening ◽

Telomere Attrition ◽

Clinical Complications

Vascular dysfunction is an early feature of diabetic vascular disease, due to increased oxidative stress and reduced nitric oxide (NO) bioavailability. This can lead to endothelial cell senescence and clinical complications such as stroke. Cells can become senescent by shortened telomeres and oxidative stress is known to accelerate telomere attrition. Sirtuin 1 (SIRT1) has been linked to vascular health by upregulating endothelial nitric oxide synthase (eNOS), suppressing oxidative stress, and attenuating telomere shortening. Accelerated leukocyte telomere attrition appears to be a feature of clinical type 2 diabetes (T2D) and therefore the telomere system may be a potential therapeutic target in preventing vascular complications of T2D. However the effect of T2D on vascular telomere length is currently unknown. We hypothesized that T2D gives rise to shortened leukocyte and vascular telomeres alongside reduced vascular SIRT1 expression and increased oxidative stress. Accelerated telomere attrition was observed in circulating leukocytes, but not arteries, in T2D compared to control rats. T2D rats had blunted arterial SIRT1 and eNOS protein expression levels which were associated with reduced antioxidant defense capacity. Our findings suggest that hyperglycemia and a deficit in vascular SIRT1per seare not sufficient to prematurely shorten vascular telomeres.

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