scholarly journals Cytoprotective Preconditioning of Osteoblast-Like Cells with N-Acetyl-L-Cysteine for Bone Regeneration in Cell Therapy

2019 ◽  
Vol 20 (20) ◽  
pp. 5199 ◽  
Author(s):  
Masahiro Yamada ◽  
Jun Watanabe ◽  
Takeshi Ueno ◽  
Takahiro Ogawa ◽  
Hiroshi Egusa
Keyword(s):  
Oxidative Stress ◽  
Cell Therapy ◽  
Bone Regeneration ◽  
Osteogenic Differentiation ◽  
Cell Tracking ◽  
Negative Impact ◽  
Redox Balance ◽  
Continuous Exposure ◽  
Osteogenic Differentiation Medium ◽  
Induced Apoptosis

Oxidative stress hinders tissue regeneration in cell therapy by inducing apoptosis and dysfunction in transplanted cells. N-acetyl-L-cysteine (NAC) reinforces cellular antioxidant capabilities by increasing a major cellular endogenous antioxidant molecule, glutathione, and promotes osteogenic differentiation. This study investigates the effects of pretreatment of osteoblast-like cells with NAC on oxidative stress-induced apoptosis and dysfunction and bone regeneration in local transplants. Rat femur bone marrow-derived osteoblast-like cells preincubated for 3 h with and without 5 mM NAC were cultured in a NAC-free osteogenic differentiation medium with continuous exposure to 50 μM hydrogen peroxide to induce oxidative stress. NAC preincubation prevented disruption of intracellular redox balance and alleviated apoptosis and negative impact on osteogenic differentiation, even under oxidative stress. Autologous osteoblast-like cells with and without NAC pretreatment in a collagen sponge vehicle were implanted in critical-size defects in rat femurs. In the third week, NAC-pretreated cells yielded complete defect closure with significantly matured lamellar bone tissue in contrast with poor bone healing by cells without pretreatment. Cell-tracking analysis demonstrated direct bone deposition by transplanted cells pretreated with NAC. Pretreatment of osteoblast-like cells with NAC enhances bone regeneration in local transplantation by preventing oxidative stress-induced apoptosis and dysfunction at the transplanted site.

scholarly journals Restoring redox balance enhances contractility in heart trabeculae from type 2 diabetic rats exposed to high glucose

2015 ◽  
Vol 308 (4) ◽  
pp. H291-H302 ◽  
Author(s):  
Niraj M. Bhatt ◽  
Miguel A. Aon ◽  
Carlo G. Tocchetti ◽  
Xiaoxu Shen ◽  
Swati Dey ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
High Glucose ◽  
Negative Impact ◽  
Antioxidant Activities ◽  
Contractile Function ◽  
Heart Function ◽  
Redox Balance ◽  
The Impact ◽  
Type 2 Diabetic

Hearts from type 2 diabetic (T2DM) subjects are chronically subjected to hyperglycemia and hyperlipidemia, both thought to contribute to oxidizing conditions and contractile dysfunction. How redox alterations and contractility interrelate, ultimately diminishing T2DM heart function, remains poorly understood. Herein we tested whether the fatty acid palmitate (Palm), in addition to its energetic contribution, rescues function by improving redox [glutathione (GSH), NAD(P)H, less oxidative stress] in T2DM rat heart trabeculae subjected to high glucose. Using cardiac trabeculae from Zucker Diabetic Fatty (ZDF) rats, we assessed the impact of low glucose (EG) and high glucose (HG), in absence or presence of Palm or insulin, on force development, energetics, and redox responses. We found that in EG ZDF and lean trabeculae displayed similar contractile work, yield of contractile work (Ycw), representing the ratio of force time integral over rate of O2 consumption. Conversely, HG had a negative impact on Ycw, whereas Palm, but not insulin, completely prevented contractile loss. This effect was associated with higher GSH, less oxidative stress, and augmented matrix GSH/thioredoxin (Trx) in ZDF mitochondria. Restoration of myocardial redox with GSH ethyl ester also rescued ZDF contractile function in HG, independently from Palm. These results support the idea that maintained redox balance, via increased GSH and Trx antioxidant activities to resist oxidative stress, is an essential protective response of the diabetic heart to keep contractile function.

Coordination of Fenretinide-Induced Apoptosis by Stress-Responsive Regulators in Leukemia Cells

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 4730-4730
Author(s):  
Kankan Wang ◽  
Hai Fang ◽  
Da-Kai Xiao ◽  
Xue-Hua Zhu ◽  
Miao- Miao He ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cancer Cells ◽  
Cell Apoptosis ◽  
Target Genes ◽  
Systems Approach ◽  
Transcriptome Profiling ◽  
Redox Balance ◽  
Pharmacological Intervention ◽  
Downstream Effects ◽  
Induced Apoptosis

Abstract Pharmacological intervention affecting intracellular redox balance often results in oxidative stress-mediated apoptosis, which also represents a new direction for cancer therapeutic designs. However, mechanistic links between redox signals and their downstream effects on apoptosis have not yet been elucidated in cancer cells. Here, we report a detailed analysis of fenretinide-induced apoptosis in leukemia-derived cells through a systems approach, integrating experimental and computational methods together with advanced data mining tools. Robust transcriptome profiling reveals numerous stress-responsive events at the temporal and spatial levels, including oxidative stress, endoplasmic reticulum stress/unfolded protein response, translational repression, proteasome activation, and apoptosis induction. Moreover, stress-responsive transcription factors, as highlighted by NRF2 and HSF1, play prominent roles in the configuration of these relevant events. Several lines of evidence suggest that these stress-responsive regulators and thus their target genes are involved not only in converting oxidative signaling into downstream effects but also in coordinating the progression of cell apoptosis. This study provides a roadmap for understanding oxidative stress-mediated apoptosis in cancer cells, which may be further developed into more sophisticated therapeutic protocols, as implicated by synergistic induction of cell apoptosis using proteasome inhibitors with fenretinide.

The role of the oral cavity immune cells in the postoperative complications after face lifting

2018 ◽  
pp. 174-178
Author(s):  
Ш.М. Абрамян ◽  
Е.В. Рожнова ◽  
Е.Н. Волкова ◽  
С.Н. Блохин ◽  
С.Г. Морозов
Keyword(s):  
Oral Cavity ◽  
Immune Cells ◽  
Postoperative Period ◽  
Negative Impact ◽  
Tooth Enamel ◽  
Healing Time ◽  
Negative Contribution ◽  
Dental Diseases ◽  
Induced Apoptosis ◽  
Wound Healing Time

Цель. Изучение клеток иммунной системы полости рта у пациентов до проведения операции лифтинга лица, а также сопоставление этих данных с показателями, выявленными при осложнениях в послеоперационном периоде. Методика. Исследованы клетки иммунной системы полости рта 100 женщин (23-68 лет), которым перед операцией лифтинга лица проведено стоматологическое обследование и необходимое лечение при наличии кариеса дентина, клиновидного дефекта эмали зуба, хронического периодонтита или пульпита. Выделенные путем смывов десенной борозды клетки окрашивали моноклональными антителами и анализировали на проточном цитометре. Определяли уровень спонтанного и индуцированного апоптоза. Оценивали уровень фагоцитоза и генерацию супероксидного аниона нейтрофилами. Результаты. Показано, что хронические воспалительные заболевания зубов оказывают негативное влияние на состояние иммунных клеток ротовой полости, сопровождаются повышением генерации супероксидного аниона нейтрофилами, повышением уровня спонтанного и церамид-индуцированного апоптоза клеток десенной борозды. Заключение. Наличие хронической патологии зубов, даже после санации, оказывает негативное влияние на течение послеоперационного периода при проведении операции лифтинга лица, в частности, способствует увеличению времени заживления операционной раны, инфицированию раны с появлением очагов некроза в области операционного шва. The object. The study of the cells of the immune system of the oral cavity in patients before the operation of face lifting, as well as a comparison of these indicators with complications in the postoperative period. Methods. The immune cells from the oral cavity were studied in 100 women (23-68 years), who underwent a dental examination and necessary treatment if they had the dentin caries, wedge-shaped defect of tooth enamel, chronic periodontitis or pulpitis before the facial lifting operation. The immune cells have been isolated by a lavage of gingival sulcus around the damaged tooth. Results. It has been shown that chronic dental diseases made a negative contribution to the oral cavity immune cells. It has been accompanied by the elevated levels of superoxide originating from neutrophils as well as the increased levels of spontaneous and ceramide-induced apoptosis of immune cells isolated from the gingival sulcus. Conclusion. The presence of chronic pathology of teeth even in the case of the preoperative dental sanation has a negative impact on the postoperative period after face lifting, in particular, contributes to the lengthening of the surgical wound healing time, wound infection as well as the partial necrosis of suture.

Hybrid Compounds & Oxidative Stress Induced Apoptosis in Cancer Therapy

2020 ◽  
Vol 27 (13) ◽  
pp. 2118-2132 ◽  
Author(s):  
Aysegul Hanikoglu ◽  
Hakan Ozben ◽  
Ferhat Hanikoglu ◽  
Tomris Ozben
Keyword(s):  
Oxidative Stress ◽  
Drug Resistance ◽  
Side Effects ◽  
Cancer Therapy ◽  
Tumor Cells ◽  
Anticancer Drugs ◽  
Chemotherapeutic Agents ◽  
Oxidation Reactions ◽  
Hybrid Compounds ◽  
Induced Apoptosis

: Elevated Reactive Oxygen Species (ROS) generated by the conventional cancer therapies and the endogenous production of ROS have been observed in various types of cancers. In contrast to the harmful effects of oxidative stress in different pathologies other than cancer, ROS can speed anti-tumorigenic signaling and cause apoptosis of tumor cells via oxidative stress as demonstrated in several studies. The primary actions of antioxidants in cells are to provide a redox balance between reduction-oxidation reactions. Antioxidants in tumor cells can scavenge excess ROS, causing resistance to ROS induced apoptosis. Various chemotherapeutic drugs, in their clinical use, have evoked drug resistance and serious side effects. Consequently, drugs having single-targets are not able to provide an effective cancer therapy. Recently, developed hybrid anticancer drugs promise great therapeutic advantages due to their capacity to overcome the limitations encountered with conventional chemotherapeutic agents. Hybrid compounds have advantages in comparison to the single cancer drugs which have usually low solubility, adverse side effects, and drug resistance. This review addresses two important treatments strategies in cancer therapy: oxidative stress induced apoptosis and hybrid anticancer drugs.

Excessive Oxidative Stress in the Synergistic Effects of Shikonin on the Hyperthermia-Induced Apoptosis

2018 ◽  
Vol 18 (5) ◽  
pp. 322-334 ◽  
Author(s):  
J.-L. Piao ◽  
Y.-J. Jin ◽  
M.-L. Li ◽  
S.A. Zakki ◽  
L. Sun ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Synergistic Effects ◽  
Induced Apoptosis

scholarly journals Redox Imbalance in T Cell-Mediated Skin Diseases

2010 ◽  
Vol 2010 ◽  
pp. 1-9 ◽  
Author(s):  
Saveria Pastore ◽  
Liudmila Korkina
Keyword(s):  
Oxidative Stress ◽  
Atopic Dermatitis ◽  
Contact Dermatitis ◽  
Skin Diseases ◽  
Redox Balance ◽  
Inflammatory Disorder ◽  
Chronic Inflammatory Disorder ◽  
Physical Chemical ◽  
Chemical Oxidants ◽  
Beneficial Outcome

The skin is permanently exposed to physical, chemical, and biological aggression by the environment. In addition, acute and chronic inflammatory events taking place in the skin are accompanied by abnormal release of pro-oxidative mediators. In this paper, we will briefly overview the homeostatic systems active in the skin to maintain the redox balance and also to counteract abnormal oxidative stress. We will concentrate on the evidence that a local and/or systemic redox dysregulation accompanies the chronic inflammatory disorder events associated to psoriasis, contact dermatitis, and atopic dermatitis. We will also discuss the fact that several well-established treatments for the therapy of chronic inflammatory skin disorders are based on the application of strong physical or chemical oxidants onto the skin, indicating that, in selected conditions, a further increase of the oxidative imbalance may lead to a beneficial outcome.

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.

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