scholarly journals Propofol Attenuates Hypoxia-Induced Inflammation in BV2 Microglia by Inhibiting Oxidative Stress and NF-κB/Hif-1α Signaling

2020 ◽  
Vol 2020 ◽  
pp. 1-11 ◽  
Author(s):  
Xiaowei Peng ◽  
Chenglong Li ◽  
Wei Yu ◽  
Shuai Liu ◽  
Yushuang Cong ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hypoxia Inducible Factor ◽  
Underlying Mechanism ◽  
Beneficial Effects ◽  
Hypoxia Inducible Factor 1 ◽  
B Subunit ◽  
Bv2 Cells ◽  
Total Antioxidant ◽  
Bv2 Microglia ◽  
Interfering Rna

Hypoxia-induced neuroinflammation typically causes neurological damage and can occur during stroke, neonatal hypoxic-ischemic encephalopathy, and other diseases. Propofol is widely used as an intravenous anesthetic. Studies have shown that propofol has antineuroinflammatory effect. However, the underlying mechanism remains to be fully elucidated. Thus, we aimed to investigate the beneficial effects of propofol against hypoxia-induced neuroinflammation and elucidated its potential cellular and biochemical mechanisms of action. In this study, we chose cobalt chloride (CoCl2) to establish a hypoxic model. We found that propofol decreased hypoxia-induced proinflammatory cytokines (TNFα, IL-1β, and IL-6) in BV2 microglia, significantly suppressed the excessive production of reactive oxygen species, and increased the total antioxidant capacity and superoxide dismutase activity. Furthermore, propofol attenuated the hypoxia-induced decrease in mitochondrial membrane potential andy 2 strongly inhibited protein expression of nuclear factor-kappa B (NF-κB) subunit p65 and hypoxia inducible factor-1α (Hif-1α) in hypoxic BV2 cells. To investigate the role of NF-κB p65, specific small interfering RNA (siRNA) against NF-κB p65 were transfected into BV2 cells, followed by exposure to hypoxia for 24 h. Hypoxia-induced Hif-1α production was downregulated after NF-κB p65 silencing. Further, propofol suppressed Hif-1α expression by inhibiting the upregulation of NF-κB p65 after exposure to hypoxia in BV2 microglia. In summary, propofol attenuates hypoxia-induced neuroinflammation, at least in part by inhibiting oxidative stress and NF-κB/Hif-1α signaling.

scholarly journals Antioxidant Potential and Peroxidative State of `Golden Smoothee' Apples Treated with 1-Methylcyclopropene

2006 ◽  
Vol 131 (1) ◽  
pp. 104-109 ◽  
Author(s):  
Rosa Vilaplana ◽  
M. Carme Valentines ◽  
Peter Toivonen ◽  
Christian Larrigaudière
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Antioxidant Activity ◽  
Storage Period ◽  
Antioxidant Potential ◽  
Total Antioxidant Activity ◽  
Pulp Tissue ◽  
Antioxidant Metabolism ◽  
Beneficial Effects ◽  
Total Antioxidant

In order to determine the effects that 1-methylcyclopropene (1-MCP) may have on antioxidant metabolism during cold storage, apples (Malus ×domestica Borkh. cv. Golden Smoothee) were treated with 625 nL·L−1 1-MCP immediately after harvest and stored in air for 3 months. Differences in total antioxidant activity and ascorbate levels were determined during storage and related to the activity of the antioxidant enzymes superoxide dismutase [SOD (EC 1.15.1.1)], catalase [CAT (EC 1.11.1.6)], and peroxidase [POX (EC 1.11.1.7)] in pulp. The level of oxidative stress in the pulp tissue was also established by determining changes in levels of hydrogen peroxide and in the content of peroxidative markers during storage. Controls and 1-MCP-treated fruit exhibited similar changes in total antioxidant activity and ascorbate levels. However, significant differences in oxidative stress levels were found between treated and untreated fruit. 1-MCP-treated fruit exhibited lower levels of hydrogen peroxide and significantly lower levels in peroxidative markers, especially at the end of the storage period. In line with this last result, 1-MCP-treated fruit also exhibited greater enzymatic antioxidant potential and, more specifically, a higher level of POX activity. Collectively, these results showed that 1-MCP did not detrimentally affect the antioxidant potential of the fruit and provided evidence to support the hypothesis that the beneficial effects of 1-MCP on ripening are not exclusively limited to its effect on ethylene, but also include direct effects on peroxidation and POX enzyme activity.

scholarly journals Aβ1–40-Induced Platelet Adhesion Is Ameliorated by Rosmarinic Acid through Inhibition of NADPH Oxidase/PKC-δ/Integrin αIIbβ3 Signaling

Antioxidants ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 1671
Author(s):  
Bo Kyung Lee ◽  
Hye Jin Jee ◽  
Yi-Sook Jung
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Nadph Oxidase ◽  
Rosmarinic Acid ◽  
Platelet Adhesion ◽  
Underlying Mechanism ◽  
Vascular Pathology ◽  
Integrin Αiibβ3 ◽  
Beneficial Effects

In platelets, oxidative stress reportedly increases platelet adhesion to vessels, thus promoting the vascular pathology of various neurodegenerative diseases, including Alzheimer’s disease. Recently, it has been shown that β-amyloid (Aβ) can increase oxidative stress in platelets; however, the underlying mechanism remains elusive. In the present study, we aimed to elucidate the signaling pathway of platelet adhesion induced by Aβ1–40, the major form of circulating Aβ, through Western blotting, immunofluorescence confocal microscopy, and fluorescence-activated cell sorting analysis. Additionally, we examined whether rosmarinic acid (RA), a natural polyphenol antioxidant, can modulate these processes. Our results show that Aβ1–40-induced platelet adhesion is mediated through NADPH oxidase/ROS/PKC-δ/integrin αIIbβ3 signaling, and these signaling pathways are significantly inhibited by RA. Collectively, these results suggest that RA may have beneficial effects on platelet-associated vascular pathology in Alzheimer’s disease.

scholarly journals Hypoxia in Obesity and Diabetes: Potential Therapeutic Effects of Hyperoxia and Nitrate

2017 ◽  
Vol 2017 ◽  
pp. 1-14 ◽  
Author(s):  
Reza Norouzirad ◽  
Pedro González-Muniesa ◽  
Asghar Ghasemi
Keyword(s):  
Diabetes Management ◽  
Hypoxia Inducible Factor ◽  
Antioxidant Properties ◽  
Therapeutic Effects ◽  
Beneficial Effects ◽  
Hypoxia Inducible Factor 1 ◽  
Obesity And Diabetes ◽  
Nitrate Therapy ◽  
Prevalence Of Obesity ◽  
Signaling Components

The prevalence of obesity and diabetes is increasing worldwide. Obesity and diabetes are associated with oxidative stress, inflammation, endothelial dysfunction, insulin resistance, and glucose intolerance. Obesity, a chronic hypoxic state that is associated with decreased nitric oxide (NO) bioavailability, is one of the main causes of type 2 diabetes. The hypoxia-inducible factor-1α(HIF-1α) is involved in the regulation of several genes of the metabolic pathways including proinflammatory adipokines, endothelial NO synthase (eNOS), and insulin signaling components. It seems that adipose tissue hypoxia and NO-dependent vascular and cellular dysfunctions are responsible for other consequences linked to obesity-related disorders. Although hyperoxia could reverse hypoxic-related disorders, it increases the production of reactive oxygen species (ROS) and decreases the production of NO. Nitrate can restore NO depletion and has antioxidant properties, and recent data support the beneficial effects of nitrate therapy in obesity and diabetes. Although it seems reasonable to combine hyperoxia and nitrate treatments for managing obesity/diabetes, the combined effects have not been investigated yet. This review discusses some aspects of tissue oxygenation and the potential effects of hyperoxia and nitrate interventions on obesity/diabetes management. It can be proposed that concomitant use of hyperoxia and nitrate is justified for managing obesity and diabetes.

scholarly journals Propofol attenuates BV2 microglia inflammation via NMDA receptor inhibition

2018 ◽  
Vol 96 (3) ◽  
pp. 241-248 ◽  
Author(s):  
Qichao Wu ◽  
Yanjun Zhao ◽  
Xiangyuan Chen ◽  
Minmin Zhu ◽  
Changhong Miao
Keyword(s):  
Nmda Receptor ◽  
Inflammatory Cytokines ◽  
Inflammatory Cytokine ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Underlying Mechanism ◽  
Enzyme Expression ◽  
Bv2 Cells ◽  
Bv2 Microglia ◽  
Pro Inflammatory Cytokines

Activated microglia, involved in the occurrence and improvement of sepsis-associated encephalopathy, can induce the expression of pro-inflammatory cytokines and pro-inflammatory enzymes, resulting in inflammation-mediated neuronal cell death. It was reported that propofol could inhibit lipopolysaccharide (LPS) induced pro-inflammatory cytokine and pro-inflammatory enzyme expression in BV2 and primary microglial cells. However, the underlying mechanism is not well known. In the present study, we investigated whether and how propofol inhibited LPS-induced the expression of pro-inflammatory cytokines and pro-inflammatory enzymes in BV2 cells. LPS induced pro-inflammatory cytokine and pro-inflammatory enzyme expression, NF-κB, extracellular regulated kinase 1/2 (ERK), calcium (Ca2+)/calmodulin-dependent protein kinase II (CaMK II) phosphorylation, and BV2 cell Ca2+ accumulation. Propofol could reverse these effects induced by LPS. MK801, an inhibitor of the NMDA receptor, could attenuate LPS-induced Ca2+ accumulation, the expression of pro-inflammatory cytokines and pro-inflammatory enzymes, and phosphorylation of NF-κB, ERK, and CaMK II, which was similar to propofol. Moreover, these effects of propofol could be counteracted by rapastinel, an activator of the NMDA receptor. The present study suggested that propofol, via inhibiting the NMDA receptor, attenuating Ca2+ accumulation, and inhibiting CaMK II, ERK1/2, and NF-κB phosphorylation, down-regulated LPS-induced pro-inflammatory cytokine and pro-inflammatory enzyme expression.

scholarly journals Effect of Lactobacillus paracasei HII01 Supplementation on Total Cholesterol, and on the Parameters of Lipid and Carbohydrate Metabolism, Oxidative Stress, Inflammation and Digestion in Thai Hypercholesterolemic Subjects

2021 ◽  
Vol 11 (10) ◽  
pp. 4333
Author(s):  
Chaiyavat Chaiyasut ◽  
Yaowalak Tirawat ◽  
Bhagavathi Sundaram Sivamaruthi ◽  
Periyanaina Kesika ◽  
Subramanian Thangaleela ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Placebo Group ◽  
Total Cholesterol ◽  
Blood Lipid ◽  
Lactobacillus Paracasei ◽  
Blood Lipid Profile ◽  
Beneficial Effects ◽  
Tnf Α ◽  
Total Antioxidant ◽  
Hypercholesterolemic Subjects

Hypercholesterolemia is one of the leading causes of cardiovascular disease. Probiotics can help to improve high blood lipid levels in hypercholesterolemia patients. Lactobacillus paracasei has been reported to have beneficial effects in several subjects; however, there is a lack of studies on Thai hypercholesterolemic subjects. Thus, this study was conducted in order to investigate the effect of L. paracasei HII01 on cholesterol, oxidative stress, and other biomarkers. Fifty-two subjects were randomized into two groups: the L. paracasei treatment group and the placebo group. The study was conducted over an intervention period of 12 weeks of supplementation. The results show that L. paracasei HII01 significantly reduced the total cholesterol (TCH), triglycerides (TGs), tumor necrosis factor (TNF)-α and lipopolysaccharide (LPS) of the patients, and increased their HDL, total antioxidant capacity (TAC) and propionic acid compared to the placebo group. Moreover, the supplementation of L. paracasei HII01 significantly increased lactic acid, IL-10 and IFN-γ, and substantially decreased malondialdehyde (MDA) at the end of the treatment. The results suggest that L. paracasei HII01 improves the blood lipid profile, reduces oxidative stress, and is beneficial for health among Thai hypercholesterolemic subjects.

scholarly journals Melatonin increases 5-flurouracil-mediated apoptosis of colorectal cancer cells through enhancing oxidative stress and downregulating survivin and XIAP

Bioimpacts ◽  
2020 ◽  
Vol 11 (4) ◽  
pp. 253-261
Author(s):  
Ainaz Mihanfar ◽  
Bahman Yousefi ◽  
Saber Ghazizadeh Darband ◽  
Shirin Sadighparvar ◽  
Mojtaba Kaviani ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Caspase 3 ◽  
Survivin Expression ◽  
Annexin V ◽  
Underlying Mechanism ◽  
Expression Levels ◽  
Beneficial Effects ◽  
Development Of Resistance

Introduction: Colorectal cancer (CRC) is one of the most lethal human malignancies with a global alarming rate of incidence. The development of resistance against common chemotherapeutics such as 5-fluorouracil (5-FU) remains a big burden for CRC therapy. Therefore, we investigated the effects of melatonin on the increasing 5-FU- mediated apoptosis and its underlying mechanism in SW-480 CRC cell line. Methods: The effects of melatonin and 5- FU, alone or in combination, on cell proliferation were evaluated using an MTT assay. Further, Annexin-V Flow cytometry was used for determining the effects of melatonin and 5-FU on the apoptosis of SW-480 cell lines. The expression levels of Bax, Bcl-2, pro-caspase-3/activated caspase 3, X-linked inhibitor of apoptosis proteins (XIAP), and survivin were measured after 48 hours incubation with drugs. Cellular levels of reactive oxygen species (ROS), catalase, superoxide dismutase and glutathione peroxidase were also evaluated. Results: Melatonin and 5-FU significantly decreased the cell proliferation of SW-480 cells. Combination of 5-FU with melatonin significantly decreased the IC50 value of 5-FU from 100 μM to 50 μM. Moreover, combination therapy increased intracellular levels of ROS and suppressed antioxidant enzymatic activities (P < 0.05). Treatment with either melatonin or 5-FU resulted in the induction of apoptosis in comparison to control (P > 0.05). XIAP and survivin expression levels potently decreased after combination treatment with melatonin and 5-FU (P < 0.05). Conclusion: We demonstrated that melatonin exerts a reversing effect on the resistance to apoptosis by targeting oxidative stress, XIAP and survivin in CRC cells. Therefore, more studies need for better understanding of underlying mechanisms for beneficial effects of combination of melatonin and 5-FU.

scholarly journals Can psychobiotics administration influence behavioral responses and physiological stress in healthy rats?

2021 ◽  
Author(s):  
Mohammad Morshedi ◽  
Khadijeh Bavafa Valenlia ◽  
Maryam Saghafi-Asl ◽  
Saeid Hadi ◽  
Vahid Hadi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Physiological Stress ◽  
Behavioral Responses ◽  
Control Group ◽  
Beneficial Effects ◽  
Disease States ◽  
Stress Markers ◽  
Total Antioxidant ◽  
Male Wistar Rats ◽  
And Control

Background: There is a well-documented cross-talk between the gut and brain. Evidence is accumulating to suggest beneficial effects of psychobiotics [prebiotics, probiotics or synbiotics] on psychological distress in disease states. However, their role in healthy status remains relatively unclear. Objectives: The present study was aimed to clarify if psychobiotics could influence behavioral responses and physiological stress in healthy rats. Methods: In the present experiment, 28 male Wistar rats were divided into four groups (healthy rats treated by Lactobacillus plantarum (L.plantarum), inulin and their combination (synbiotic) and control group). Then, psychobiotics were administered to the intervention groups for 8 weeks. Behavioral tests (Morris water maze, Elevated plus maze, and Forced swimming test) were performed at the endpoint. Then, serum and brain levels of superoxide dismutase, malondialdehyde, glutathione peroxidase, total antioxidant capacity, brain-derived neurotrophic factor (BDNF), and serotonin were measured. Results: Our finding indicated that unlike inulin, the administration of L.plantarum and synbiotic could ameliorate depression and anxiety-like behavior and cognitive performance (P<0.05). Serum and brain oxidative stress markers were significantly improved by synbiotic consumption. Intake of L.plantarum led to decreased oxidative stress in the hippocampus and amygdala (P<0.05). Moreover, a significant increase in hippocampal serotonin and BDNF concentration was observed after synbiotic and L.plantarum intake (P<0.05). In addition, there was a strong correlation of serum and brain markers with behavioral performance (P< 0.05). Conclusion: Our study suggests that psychobiotics therapy may have favorable effects on the amelioration of psychological disorders.

scholarly journals HIF1 and ID1 Interplay Confers Adaptive Survival to HIF1α-Inhibition

2021 ◽  
Vol 9 ◽  
Author(s):  
Hao Geng ◽  
Hyun-Kyung Ko ◽  
Janet Pittsenbarger ◽  
Christopher T. Harvey ◽  
Changhui Xue ◽  
...  
Keyword(s):  
Hypoxia Inducible Factor ◽  
Underlying Mechanism ◽  
Glutamine Metabolism ◽  
Pathological Feature ◽  
Hypoxia Inducible Factor 1 ◽  
Promising Therapeutic Target ◽  
Hypoxic Tumor ◽  
Oncogenic Protein

Hypoxia is a universal pathological feature of solid tumors. Hypoxic tumor cells acquire metastatic and lethal phenotypes primarily through the activities of hypoxia-inducible factor 1 alpha (HIF1α). Therefore, HIF1α is considered as a promising therapeutic target. However, HIF inhibitors have not proven to be effective in clinical testing. The underlying mechanism is unclear. We report that oncogenic protein ID1 is upregulated in hypoxia by HIF1α shRNA or pharmacological inhibitors. In turn, ID1 supports tumor growth in hypoxia in vitro and in xenografts in vivo, conferring adaptive survival response and resistance. Mechanistically, ID1 proteins interfere HIF1-mediated gene transcription activation, thus ID1 protein degradation is accelerated by HIF1α-dependent mechanisms in hypoxia. Inhibitions of HIF1α rescues ID1, which compensates the loss of HIF1α by the upregulation of GLS2 and glutamine metabolism, thereby switching the metabolic dependency of HIF1α -inhibited cells from glucose to glutamine.

Oxidative stress and hypoxia inducible factor-1 alpha regulation

2007 ◽  
Vol 205 (3) ◽  
pp. S56
Author(s):  
Edward I. Chang ◽  
Eric I. Chang ◽  
Shang A. Loh ◽  
Michael G. Galvez ◽  
Geoffrey C. Gurtner
Keyword(s):  
Oxidative Stress ◽  
Hypoxia Inducible Factor ◽  
Hypoxia Inducible Factor 1

scholarly journals Hypoxia Inhibits Cavin-1 and Cavin-2 Expression and Down-Regulates Caveolae in Adipocytes

Endocrinology ◽  
2015 ◽  
Vol 156 (3) ◽  
pp. 789-801 ◽  
Author(s):  
Claire Regazzetti ◽  
Karine Dumas ◽  
Sandra Lacas-Gervais ◽  
Faustine Pastor ◽  
Pascal Peraldi ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Insulin Signaling ◽  
Hypoxia Inducible Factor ◽  
Insulin Receptors ◽  
Underlying Mechanism ◽  
Epididymal Adipose Tissue ◽  
Diabetic Patients ◽  
Model Assessment ◽  
Hypoxia Inducible Factor 1

Abstract During obesity, a hypoxic state develops within the adipose tissue, resulting in insulin resistance. To understand the underlying mechanism, we analyzed the involvement of caveolae because they play a crucial role in the activation of insulin receptors. In the present study, we demonstrate that in 3T3-L1 adipocytes, hypoxia induces the disappearance of caveolae and inhibits the expression of Cavin-1 and Cavin-2, two proteins necessary for the formation of caveolae. In mice, hypoxia induced by the ligature of the spermatic artery results in the decrease of cavin-1 and cavin-2 expression in the epididymal adipose tissue. Down-regulation of the expression of cavins in response to hypoxia is dependent on hypoxia-inducible factor-1. Indeed, the inhibition of hypoxia-inducible factor-1 restores the expression of cavins and caveolae formation. Expression of cavins regulates insulin signaling because the silencing of cavin-1 and cavin-2 impairs insulin signaling pathway. In human, cavin-1 and cavin-2 are decreased in the sc adipose tissue of obese diabetic patients compared with lean subjects. Moreover, the expression of cavin-2 correlates negatively with the homeostatic model assessment index of insulin resistance and glycated hemoglobin level. In conclusion, we propose a new mechanism in which hypoxia inhibits cavin-1 and cavin-2 expression, resulting in the disappearance of caveolae. This leads to the inhibition of insulin signaling and the establishment of insulin resistance.

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