scholarly journals Tart Cherry Extracts Reduce Inflammatory and Oxidative Stress Signaling in Microglial Cells

Antioxidants ◽  
2016 ◽  
Vol 5 (4) ◽  
pp. 33 ◽  
Author(s):  
Barbara Shukitt-Hale ◽  
Megan Kelly ◽  
Donna Bielinski ◽  
Derek Fisher
Keyword(s):  
Oxidative Stress ◽  
Microglial Cells ◽  
Stress Signaling ◽  
Tart Cherry ◽  
And Oxidative Stress

Mesenchymal stem cells inhibited the inflammation and oxidative stress in LPS-activated microglial cells through AMPK pathway

2019 ◽  
Vol 126 (12) ◽  
pp. 1589-1597 ◽  
Author(s):  
Dayong Cao ◽  
Haowen Qiao ◽  
Dejiao He ◽  
Xingping Qin ◽  
Qian Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Microglial Cells ◽  
Ampk Pathway ◽  
And Oxidative Stress

Oxidative Stress Signaling Pathway of Heme Regulated eIF2α Kinase in mitigating the Severity of β-Thalassemia

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 127-127 ◽  
Author(s):  
Rajasekhar NVS Suragani ◽  
Sijin Liu ◽  
Wanting Zhao ◽  
Jane-Jane Chen
Keyword(s):  
Oxidative Stress ◽  
Protein Synthesis ◽  
Stress Response ◽  
Signaling Pathway ◽  
Fetal Liver ◽  
Stress Signaling ◽  
Erythroid Precursors ◽  
Inhibition Of Protein Synthesis ◽  
And Oxidative Stress ◽  
Stress Signaling Pathway

Abstract Maturation of erythroid precursors requires active synthesis of hemoglobin which consists of two pairs of α- and β-globin subunits with each monomer bound to a heme moiety. Heme Regulated Inhibitor (HRI) is the only eIF2αkinase responsible for the balanced synthesis of heme and globin at translational level in erythroid cells. Activation of HRI in heme deficiency leads to phosphorylation of the α-subunit of eukaryotic initiation factor (eIF2α) and inhibition of protein synthesis. HRI is also activated by denatured proteins and oxidative stress. In addition to general inhibition of protein synthesis, phosphorylation of eIF2α (eIF2αP) also leads to the induction of a stress signaling pathway. Activating transcription factor 4 (Atf4) mRNA is preferentially translated amidst global inhibition of protein synthesis. Atf4 activates transcription of stress response proteins, Chop (CCAAT/enhancer binding protein homologous protein-10) and the non-enzymatic cofactor of eIF2α phosphatase (PP1A) Gadd34. These stress response proteins help cells in mitigating the stress. While the role of HRI in translational regulation of non-nucleated reticulocytes is well established, the HRIdependent Atf4 stress signaling pathway of nucleated erythroid precursors is unknown. Sodium arsenite toxicity was used as a model system of oxidative stress to elucidate the HRI signaling pathway in Hri +/+ and −/− E14.5 mouse fetal liver erythroid precursors. In HRI deficiency, erythroid precursors were more sensitive to arsenite toxicity with decreased cell viability and increased apoptosis, by caspase 3 executed intrinsic apoptotic pathway. HRI was activated by autophosphorylation as early as 15 minutes following arsenite treatment. In addition to increased eIF2αP, there was induction of Atf4, Chop and Gadd34 in Hri+/+ fetal liver cells. Importantly, in Hri−/− cells neither the phosphorylation of eIF2α nor the expression of Atf4, Chop and Gadd34 was increased upon arsenite treatment. In addition, we also observed HRI dependent induction of Heme Oxygenase 1 (HO-1) that plays a pivotal role in adaptation to oxidative stress. These results demonstrate that HRI induces a signaling pathway for adaptive gene expression to protect the nucleated erythroid precursors from apoptosis upon oxidative stress. Iron overload, accumulation of unpaired α-globin and oxidative stress are well documented in β-thalassemia. Recently, HRI was discovered to be necessary for the survival of β-thalassemic mice. β-thalassemic mice lacking one copy of HRI (Hri+/− Hbb−/−) also manifest a more severe syndrome of the disease. We have investigated the activation of eIF2αP/Atf4 signaling pathway in Hri+/−Hbb−/− β-thalassemic erythroid cells using eIF2αP phosphatase (Gadd34) inhibitor salubrinal. Treatment of reticulocytes from Hri+/−Hbb−/− mice with salubrinal increased eIF2αP and resulted in inhibition of newly synthesized globin protein synthesis. The decreased globin protein synthesis also resulted in decreased aggregation of the unpaired α-globins. Furthermore, treatment of salubrinal in nucleated fetal liver erythroblasts also increased Chop expression and decreased apoptosis. Thus, activation of the eIF2αP/Atf4 pathway by small chemicals might be a novel pharmaceutical approach to decrease proteotoxicity and apoptosis for the treatment of β-thalassemia.

Efficacy Of Tart Cherry Juice In Reducing Muscle Damage, Inflammation And Oxidative Stress Following Marathon Running

2009 ◽  
Vol 41 ◽  
pp. 507-508 ◽  
Author(s):  
Glyn Howatson ◽  
Malachy P. McHugh ◽  
Jessica L. Hill ◽  
James Brouner ◽  
Andy P. Jewell ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Muscle Damage ◽  
Marathon Running ◽  
Tart Cherry ◽  
Cherry Juice ◽  
And Oxidative Stress

Oxidative signalling and inflammatory pathways in Alzheimer's disease

2001 ◽  
Vol 67 ◽  
pp. 141-149 ◽  
Author(s):  
Ian Anderson ◽  
Christy Adinolfi ◽  
Susan Doctrow ◽  
Karl Huffman ◽  
Ken A. Joy ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Neuronal Cell ◽  
Amyloid Peptide ◽  
Microglial Cells ◽  
Amino Acid Form ◽  
Factor Α ◽  
Molecular Components ◽  
And Oxidative Stress

It is well established that inflammation and oxidative stress are key components of the pathology of Alzheimer's disease (AD), but how early in the pathological cascade these processes are involved or which specific molecular components are key, has not been fully elucidated. This paper describes the pharmacological approach to understand the molecular components of inflammation and oxidative stress on the activation of microglial cells and neuronal cell viability. We have shown that activation of microglia with the 42-amino-acid form of the ϐ-amyloid peptide (Aϐ42) activates the production of cyclooxygenase-2, the inducible form of nitric oxide synthase and tumour necrosis factor-α and there appears to be little interactive feedback between these three mediators. Moreover, we explore the effects of a series of salen-manganese complexes, EUK-8, -134 and -189, which are known to possess both superoxide and catalase activity. These compounds are able to protect cells from insults produced by hydrogen peroxide or peroxynitrite. Moreover, EUK-134 was also able to limit the output of prostaglandin E2 from activated microglial cells. The mechanisms underlying these effects are discussed. Together, these data support a pivotal role for oxidative stress and inflammation as key mediators of the pathological cascade in AD and provide some ideas about possible therapeutic targets.

scholarly journals Effects of Tart Cherry Juice on Biomarkers of Inflammation and Oxidative Stress in Older Adults

Nutrients ◽  
2019 ◽  
Vol 11 (2) ◽  
pp. 228 ◽  
Author(s):  
Sheau Chai ◽  
Kristina Davis ◽  
Zugui Zhang ◽  
Longying Zha ◽  
Kenneth Kirschner
Keyword(s):  
Oxidative Stress ◽  
Ldl Cholesterol ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Significant Group Effect ◽  
Tart Cherry ◽  
Blood Biomarkers ◽  
Significant Group ◽  
Cherry Juice ◽  
And Oxidative Stress

Inflammation and oxidative stress are important factors in the development of cardiovascular disease and atherosclerosis. The findings of our previous study suggest that 12 weeks consumption of tart cherry juice lowers the levels of systolic blood pressure (BP) and low-density lipoprotein (LDL) cholesterol in older adults. The present study investigated the effects of tart cherry juice on blood biomarkers of inflammation and oxidative stress. In this randomized-controlled clinical trial, a total of 37 men and women between the ages of 65–80 were randomly assigned to consume 480 mL of tart cherry juice or control drink daily for 12 weeks. Several blood biomarkers of inflammation and oxidative stress were assessed at baseline and after 12 weeks intervention. After the 12 weeks intervention, tart cherry juice significantly increased the plasma levels of DNA repair activity of 8-oxoguanine glycosylase (p < 0.0001) and lowered (p = 0.03) the mean c-reactive protein (CRP) level compared to the control group. There was a significant group effect observed for plasma CRP (p = 0.03) and malondialdehyde (MDA) (p = 0.03), and a borderline significant group effect observed for plasma oxidized low-density lipoprotein (OxLDL) (p = 0.07). Within group analysis showed that the plasma levels of CRP, MDA, and OxLDL decreased numerically by 25%, 3%, and 11%, respectively after 12 weeks of tart cherry juice consumption compared with corresponding baseline values. The present study suggests that the ability of tart cherry juice to reduce systolic BP and LDL cholesterol, in part, may be due to its anti-oxidative and anti-inflammatory properties. Larger and longer follow-up studies are needed to confirm these findings.

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