Umbilical Cord Mesenchymal Stem Cell Exosomes Alleviate the Progression of Kidney Failure by Modulating Inflammatory Responses and Oxidative Stress in an Ischemia-Reperfusion Mice Model

2021 ◽  
Vol 17 (9) ◽  
pp. 1874-1881
Author(s):  
Yanqiang Zhang ◽  
Chongjuan Wang ◽  
Zhuxiao Bai ◽  
Peng Li
Keyword(s):  
Oxidative Stress ◽  
Stem Cells ◽  
Renal Failure ◽  
Stem Cell ◽  
Protein Expression ◽  
Inflammatory Responses ◽  
Ischemia Reperfusion ◽  
Protein Expression Level ◽  
M1 Macrophages ◽  
And Oxidative Stress

The efficacy of stem cells for the treatment of renal failure is widely recognized; however, an excessive volume of stem cells can block the capillaries; thus, the potential risks should not be ignored. Stem cell exosomes are secretory extracellular vesicles with a size of 30–150 nm, which have similar functions to stem cells but are much smaller in size. This study aims to investigate the role of human umbilical cord mesenchymal stem cells (UCMSCs)-derived exosomes in the treatment of renal failure caused by ischemia-reperfusion. Fifty 8-week-old female C57 mice underwent bilateral renal ischemia-reperfusion surgery for 30 minutes. After 4 weeks, the treated group received UCMSCs-derived exosomes treatment, and the control group was solely injected with the same amount of PBS. At the age of 16 weeks, the kidney function, kidney damage, inflammatory responses and oxidative stress were measured. Moreover, the effect of UCMSCs-derived exosomes on the phenotype of M1 macrophages was also tested. The results showed that UCMSCsderived exosomes significantly reduced the levels of blood urea nitrogen (BUN), serum creatinine (SCR), and urinary albumin and creatinine (ACR) and 8-isoprostane. UCMSCs-derived exosomes also improved the atrophy of the kidney and glomerulus, decreased kidney pro-inflammatory factors expression (mRNA of II-1β, II-6, Tnf-α, and Mcp-1) and oxidative stress (malondialdehyde), and increased glutathione level. However, F4/80 immunohistochemistry did not show significant differences between the two groups. In systemic inflammation measurement, UCMSCs-derived exosomes decreased proinflammatory factors TNF-α, IL-6, and IL-1β levels, and increased anti-inflammatory factor IL-10 level. In vitro experiments showed that UCMSCs-derived exosomes decreased the protein expression level of TNF-α and increased the protein expression level of IL-10 in M1 macrophages. UCMSCs-derived exosomes reduce kidney inflammation and oxidative stress by improving systemic inflammation, and thus reduce kidney damage and improve kidney function. This study shows the potential application value of exosomes in the treatment of renal failure.

scholarly journals Ultraviolet Radiation-Induced Skin Aging: The Role of DNA Damage and Oxidative Stress in Epidermal Stem Cell Damage Mediated Skin Aging

2016 ◽  
Vol 2016 ◽  
pp. 1-14 ◽  
Author(s):  
Uraiwan Panich ◽  
Gunya Sittithumcharee ◽  
Natwarath Rathviboon ◽  
Siwanon Jirawatnotai
Keyword(s):  
Oxidative Stress ◽  
Stem Cells ◽  
Dna Damage ◽  
Mesenchymal Stem Cells ◽  
Stem Cell ◽  
Ultraviolet Radiation ◽  
Skin Aging ◽  
The Body ◽  
And Oxidative Stress

Skin is the largest human organ. Skin continually reconstructs itself to ensure its viability, integrity, and ability to provide protection for the body. Some areas of skin are continuously exposed to a variety of environmental stressors that can inflict direct and indirect damage to skin cell DNA. Skin homeostasis is maintained by mesenchymal stem cells in inner layer dermis and epidermal stem cells (ESCs) in the outer layer epidermis. Reduction of skin stem cell number and function has been linked to impaired skin homeostasis (e.g., skin premature aging and skin cancers). Skin stem cells, with self-renewal capability and multipotency, are frequently affected by environment. Ultraviolet radiation (UVR), a major cause of stem cell DNA damage, can contribute to depletion of stem cells (ESCs and mesenchymal stem cells) and damage of stem cell niche, eventually leading to photoinduced skin aging. In this review, we discuss the role of UV-induced DNA damage and oxidative stress in the skin stem cell aging in order to gain insights into the pathogenesis and develop a way to reduce photoaging of skin cells.

(Z)-7,4′-Dimethoxy-6-hydroxy-aurone- 4-O-β-glucopyranoside alleviates cerebral ischemia-reperfusion injury in rats associating with the regulation of JAK1/STAT1 signaling pathway

2020 ◽  
Vol 39 (11) ◽  
pp. 1507-1517
Author(s):  
R Du ◽  
X Zhou ◽  
D Yang ◽  
H Zhou ◽  
F Lin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cerebral Ischemia ◽  
Protein Expression ◽  
Inflammatory Responses ◽  
Ischemia Reperfusion ◽  
Janus Kinase ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Enzyme Linked Immunosorbent Assay ◽  
Cerebral Ischemia Reperfusion ◽  
Brain Tissues

Inflammatory responses have been demonstrated to contribute to the neuronal death following cerebral ischemia. This study was to investigate the repairing effects and potential mechanisms of (Z)-7,4′-dimethoxy-6-hydroxy-aurone-4-O-β-glucopyranoside (DHAG), a compound with neuroprotective effects, on cerebral ischemia-reperfusion (I/R) injury in rats. Cerebral I/R model was established with middle cerebral artery occlusion method in Sprague Dawley rats and then rats were treated with DHAG (1 and 2 mg/kg) for 7 days. The volume of cerebral infarction was detected by triphenyltetrazolium chloride staining. The apoptosis in ischemic brain tissues was detected by terminal deoxynucleotidyl transferase dUTP nick end labeling assay. Oxidative stress markers and inflammatory factors were detected by enzyme-linked immunosorbent assay. Protein expression was detected by Western blot. DHAG treatment significantly alleviated the cerebral I/R injury and decreased apoptosis in brain tissues. Moreover, DHAG treatment significantly inhibited oxidative stress and reduced inflammatory responses, associating with decreasing the protein expression of phosphorylated Janus kinase 1/phosphorylated signal transducer and transcriptional activator 1. These results demonstrated neuroprotective properties of DHAG and highlighted it as a potential therapeutic agent against injury of cerebral IR.

scholarly journals Polyurethane–polylactide-based material doped with resveratrol decreases senescence and oxidative stress of adipose-derived mesenchymal stromal stem cell (ASCs)

RSC Advances ◽  
2017 ◽  
Vol 7 (39) ◽  
pp. 24070-24084 ◽  
Author(s):  
K. Kornicka ◽  
D. Nawrocka ◽  
A. Lis-Bartos ◽  
M. Marędziak ◽  
K. Marycz
Keyword(s):  
Oxidative Stress ◽  
Tissue Engineering ◽  
Stem Cells ◽  
Stem Cell ◽  
Stress Factor ◽  
Adipose Derived Stem Cells ◽  
Stromal Stem Cell ◽  
Mesenchymal Stromal Stem Cell ◽  
And Oxidative Stress

The aim of this study was to evaluate the influence of resveratrol (RES)-doped polyurethane (TPU)–polylactide (PLA) biomaterials on the senescence and oxidative stress factor of adipose-derived stem cells (ASCs) for tissue engineering.

scholarly journals Anti-Aging Effect of the Ketone Metabolite β-Hydroxybutyrate in Drosophila Intestinal Stem Cells

2020 ◽  
Vol 21 (10) ◽  
pp. 3497 ◽  
Author(s):  
Joung-Sun Park ◽  
Yung-Jin Kim
Keyword(s):  
Oxidative Stress ◽  
Stem Cells ◽  
Stem Cell ◽  
Adult Stem Cells ◽  
Intestinal Stem Cells ◽  
Aging Effects ◽  
Age Related ◽  
Tissue Aging ◽  
And Oxidative Stress ◽  
Age Related Changes

Age-related changes in tissue-resident adult stem cells may be closely linked to tissue aging and age-related diseases, such as cancer. β-Hydroxybutyrate is emerging as an important molecule for exhibiting the anti-aging effects of caloric restriction and fasting, which are generally considered to be beneficial for stem cell maintenance and tissue regeneration. The effects of β-hydroxybutyrate on adult stem cells remain largely unknown. Therefore, this study was undertaken to investigate whether β-hydroxybutyrate supplementation exerts beneficial effects on age-related changes in intestinal stem cells that were derived from the Drosophila midgut. Our results indicate that β-hydroxybutyrate inhibits age- and oxidative stress-induced changes in midgut intestinal stem cells, including centrosome amplification (a hallmark of cancers), hyperproliferation, and DNA damage accumulation. Additionally, β-hydroxybutyrate inhibits age- and oxidative stress-induced heterochromatin instability in enterocytes, an intestinal stem cells niche cells. Our results suggest that β-hydroxybutyrate exerts both intrinsic as well as extrinsic influence in order to maintain stem cell homeostasis.

scholarly journals Impact of Magnetic Labeling on Human and Mouse Stem Cells and Their Long-Term Magnetic Resonance Tracking in a Rat Model of Parkinson Disease

2009 ◽  
Vol 8 (3) ◽  
pp. 7290.2009.00017 ◽  
Author(s):  
Albrecht Stroh ◽  
Johannes Boltze ◽  
Katharina Sieland ◽  
Katharina Hild ◽  
Cindy Gutzeit ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stem Cells ◽  
Stem Cell ◽  
Iron Oxide ◽  
Magnetic Resonance ◽  
Rat Model ◽  
Stress Levels ◽  
Magnetic Labeling ◽  
The Impact ◽  
And Oxidative Stress

Magnetic resonance imaging (MRI) of magnetically labeled stem cells has become a valuable tool in the understanding and evaluation of experimental stem cell–based therapies of degenerative central nervous system disorders. This comprehensive study assesses the impact of magnetic labeling of both human and rodent stem cell–containing populations on multiple biologic parameters as maintenance of stemness and oxidative stress levels. Cells were efficiently magnetically labeled with very small superparamagnetic iron oxide particles. Only under the condition of tailored labeling strategies can the impact of magnetic labeling on vitality, proliferation, pluripotency, and oxidative stress levels be minimized. In a rat model of Parkinson disease, magnetically labeled mouse embryonic stem cells were tracked by high-field MRI for 6 months. Significant interindividual differences concerning the spatial distribution of cells became evident. Histologically, transplanted green fluorescent protein–positive iron oxide–labeled cells were clearly identified. No significant increase in oxidative stress levels at the implantation site and no secondary uptake of magnetic label by host phagocytotic cells were observed. Our study strongly suggests that molecular MRI approaches must be carefully tailored to the respective cell population to exert minimal physiologic impact, ensuring the feasibility of this imaging approach for clinical applications.

Effects of Off-Pump Versus On-Pump Coronary Artery Bypass Grafting: Apoptosis, Inflammation, and Oxidative Stress

2014 ◽  
Vol 17 (5) ◽  
pp. 271 ◽  
Author(s):  
Murat Bicer ◽  
Tunay Senturk ◽  
Murat Yanar ◽  
Ahmet Tutuncu ◽  
Arzu Yilmaztepe Oral ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Ischemia Reperfusion ◽  
Artery Bypass ◽  
Bypass Grafting ◽  
Artery Bypass Grafting ◽  
Cabg Surgery ◽  
Off Pump ◽  
Pump Cabg ◽  
Hs Crp ◽  
And Oxidative Stress

<strong>Background</strong>: It has been suggested that off-pump coronary<br />artery bypass grafting (CABG) surgery reduces myocardial<br />ischemia-reperfusion injury, postoperative systemic<br />inflammatory response, and oxidative stress. The aim of this<br />study was to measure serum malondialdehyde (MDA), highsensitivity<br />C-reactive protein (hs-CRP), M30, and M65 levels<br />and to investigate the relationship between M30 levels and<br />oxidative stress and inflammation in patients undergoing onand<br />off-pump CABG surgery.<br /><strong>Methods</strong>: Fifty patients were randomly assigned to onpump<br />or off-pump CABG surgery (25 patients off-pump and<br />25 on-pump CABG surgery), and blood samples were collected<br />prior to surgery, and 30 minutes, 60 minutes, 6 hours,<br />and 24 hours after CABG surgery.<br /><strong>Results</strong>: Compared to the on-pump group, serum MDA<br />levels at 30 minutes, 60 minutes, 6 hours, and 24 hours after<br />the CABG surgery were significantly lower in the off-pump<br />group (P = .001, P = .001, P = .001, and P = .001, respectively).<br />Serum M30 levels were found to be elevated in both groups,<br />returning to baseline at 24 hours. When compared to baseline,<br />the hs-CRP level reached its peak at 24 hours at 13.28 ±<br />5.32 mg/dL in the on-pump group, and 15.44 ± 4.02 mg/dL<br />in the off-pump group.<br /><strong>Conclusion</strong>: CABG surgery is associated with an increase<br />in inflammatory markers and serum M30 levels, indicating<br />epithelial/endothelial apoptosis in the early period.

LncRNA SNHG12 Improves Cerebral Ischemic-reperfusion Injury by Activating SIRT1/FOXO3a Pathway through I nhibition of Autophagy and Oxidative Stress

2020 ◽  
Vol 17 (4) ◽  
pp. 394-401
Author(s):  
Yuanhua Wu ◽  
Yuan Huang ◽  
Jing Cai ◽  
Donglan Zhang ◽  
Shixi Liu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Molecular Mechanisms ◽  
Ischemia Reperfusion ◽  
Critical Role ◽  
Cell Activity ◽  
Ht22 Cells ◽  
Cerebral Ischemic ◽  
Cerebral Ischemic Reperfusion ◽  
And Oxidative Stress

Background: Ischemia/reperfusion (I/R) injury involves complex biological processes and molecular mechanisms such as autophagy. Oxidative stress plays a critical role in the pathogenesis of I/R injury. LncRNAs are the regulatory factor of cerebral I/R injury. Methods: This study constructs cerebral I/R model to investigate role of autophagy and oxidative stress in cerebral I/R injury and the underline regulatory mechanism of SIRT1/ FOXO3a pathway. In this study, lncRNA SNHG12 and FOXO3a expression was up-regulated and SIRT1 expression was down-regulated in HT22 cells of I/R model. Results: Overexpression of lncRNA SNHG12 significantly increased the cell viability and inhibited cerebral ischemicreperfusion injury induced by I/Rthrough inhibition of autophagy. In addition, the transfected p-SIRT1 significantly suppressed the release of LDH and SOD compared with cells co-transfected with SIRT1 and FOXO3a group and cells induced by I/R and transfected with p-SNHG12 group and overexpression of cells co-transfected with SIRT1 and FOXO3 further decreased the I/R induced release of ROS and MDA. Conclusion: In conclusion, lncRNA SNHG12 increased cell activity and inhibited oxidative stress through inhibition of SIRT1/FOXO3a signaling-mediated autophagy in HT22 cells of I/R model. This study might provide new potential therapeutic targets for further investigating the mechanisms in cerebral I/R injury and provide.

scholarly journals Fucoxanthin Ameliorates Oxidative Stress and Airway Inflammation in Tracheal Epithelial Cells and Asthmatic Mice

Cells ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 1311
Author(s):  
Shu-Ju Wu ◽  
Chian-Jiun Liou ◽  
Ya-Ling Chen ◽  
Shu-Chen Cheng ◽  
Wen-Chung Huang
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cells ◽  
Airway Inflammation ◽  
Inflammatory Cytokines ◽  
Inflammatory Responses ◽  
Therapeutic Potential ◽  
Eosinophil Infiltration ◽  
Tracheal Epithelial Cells ◽  
Tracheal Epithelial ◽  
And Oxidative Stress

Fucoxanthin is isolated from brown algae and was previously reported to have multiple pharmacological effects, including anti-tumor and anti-obesity effects in mice. Fucoxanthin also decreases the levels of inflammatory cytokines in the bronchoalveolar lavage fluid (BALF) of asthmatic mice. The purpose of the present study was to investigate the effects of fucoxanthin on the oxidative and inflammatory responses in inflammatory human tracheal epithelial BEAS-2B cells and attenuated airway hyperresponsiveness (AHR), airway inflammation, and oxidative stress in asthmatic mice. Fucoxanthin significantly decreased monocyte cell adherence to BEAS-2B cells. In addition, fucoxanthin inhibited the production of pro-inflammatory cytokines, eotaxin, and reactive oxygen species in BEAS-2B cells. Ovalbumin (OVA)-sensitized mice were treated by intraperitoneal injections of fucoxanthin (10 mg/kg or 30 mg/kg), which significantly alleviated AHR, goblet cell hyperplasia and eosinophil infiltration in the lungs, and decreased Th2 cytokine production in the BALF. Furthermore, fucoxanthin significantly increased glutathione and superoxide dismutase levels and reduced malondialdehyde (MDA) levels in the lungs of asthmatic mice. These data demonstrate that fucoxanthin attenuates inflammation and oxidative stress in inflammatory tracheal epithelial cells and improves the pathological changes related to asthma in mice. Thus, fucoxanthin has therapeutic potential for improving asthma.

scholarly journals Coptisine Attenuates Diabetes—Associated Endothelial Dysfunction through Inhibition of Endoplasmic Reticulum Stress and Oxidative Stress

Molecules ◽  
2021 ◽  
Vol 26 (14) ◽  
pp. 4210
Author(s):  
Yan Zhou ◽  
Chunxiu Zhou ◽  
Xutao Zhang ◽  
Chi Teng Vong ◽  
Yitao Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Risk Factors ◽  
Endoplasmic Reticulum ◽  
Er Stress ◽  
Vascular Function ◽  
Inflammatory Responses ◽  
Therapeutic Potential ◽  
Ex Vivo ◽  
Diabetic Mice ◽  
And Oxidative Stress

Coptisine is the major bioactive protoberberine alkaloid found in Rhizoma Coptidis. Coptisine reduces inflammatory responses and improves glucose tolerance; nevertheless, whether coptisine has vasoprotective effect in diabetes is not fully characterized. Conduit arteries including aortas and carotid arteries were obtained from male C57BL/6J mice for ex vivo treatment with risk factors (high glucose or tunicamycin) and coptisine. Some arterial rings were obtained from diabetic mice, which were induced by high-fat diet (45% kcal% fat) feeding for 6 weeks combined with a low-dose intraperitoneal injection of streptozotocin (120 mg/kg). Functional studies showed that coptisine protected endothelium-dependent relaxation in aortas against risk factors and from diabetic mice. Coptisine increased phosphorylations of AMPK and eNOS and downregulated the endoplasmic reticulum (ER) stress markers as determined by Western blotting. Coptisine elevates NO bioavailability and decreases reactive oxygen species level. The results indicate that coptisine improves vascular function in diabetes through suppression of ER stress and oxidative stress, implying the therapeutic potential of coptisine to treat diabetic vasculopathy.

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