scholarly journals Lysosome Dysfunction Enhances Oxidative Stress-Induced Apoptosis through Ubiquitinated Protein Accumulation in Hela Cells

2012 ◽  
Vol 296 (1) ◽  
pp. 31-39 ◽  
Author(s):  
Chunyan Yu ◽  
Xiaowei Huang ◽  
Ye Xu ◽  
Hongyan LI ◽  
Jing Su ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hela Cells ◽  
Protein Accumulation ◽  
Ubiquitinated Protein ◽  
Induced Apoptosis

The involvement of oxidative stress in tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL)-induced apoptosis in HeLa cells

2002 ◽  
Vol 182 (1) ◽  
pp. 75-82 ◽  
Author(s):  
Myoung Woo Lee ◽  
Soon Cheol Park ◽  
Joung-Hun Kim ◽  
In-Ki Kim ◽  
Kun Soo Han ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Tumor Necrosis Factor ◽  
Hela Cells ◽  
Tumor Necrosis ◽  
Induced Apoptosis ◽  
Necrosis Factor

scholarly journals Regional astrocyte interferon-γ signaling regulates immunoproteasome-mediated protection during chronic autoimmunity

2019 ◽  
Author(s):  
Brandon C. Smith ◽  
Maksim Sinyuk ◽  
Julius E. Jenkins ◽  
Morgan W. Psenicka ◽  
Jessica L. Williams
Keyword(s):  
Oxidative Stress ◽  
Spinal Cord ◽  
Chronic Phase ◽  
Interferon Γ ◽  
Lesion Size ◽  
Protective Role ◽  
Protein Accumulation ◽  
Ubiquitinated Protein ◽  
Human Spinal Cord

AbstractIn early autoimmune neuroinflammation, interferon (IFN)γ and its upregulation of the immunoproteasome (iP) is pathologic. However, during chronic multiple sclerosis (MS), IFNγ has protective properties and, the role of the iP remains to be fully elucidated. Here, we demonstrated that IFNγ signaling in regional astrocytes induces the iP and protects the CNS during autoimmunity. In MS tissue, iP expression was enhanced in spinal cord compared to brainstem lesions, which correlated with a decrease in oxidative stress. In vitro, IFNγ stimulation enhanced iP expression, reduced reactive oxygen species burden, and decreased oxidatively damaged and poly-ubiquitinated protein accumulation preferentially in human spinal cord astrocytes, which was abrogated with the use of the iP inhibitor, ONX 0914. During the chronic phase of an MS animal model, experimental autoimmune encephalomyelitis (EAE), ONX 0914 treatment exacerbated disease and led to increased oxidative stress and poly-ubiquitinated protein build-up. Finally, mice with astrocyte-specific loss of the IFNγ receptor exhibited worsened chronic EAE associated with reduced iP expression, enhanced lesion size and oxidative stress and poly-ubiquitinated protein accumulation in astrocytes. Taken together, our data reveal a protective role for IFNγ in chronic neuroinflammation and identify a novel function of the iP in astrocytes during CNS autoimmunity.

scholarly journals NF-κB, Caspase-3 and p53 Pathways are Involved in Resveratrol-Chitosan Nanoparticles-Induced Apoptosis in Hela Cells with Oxidative Stress

2021 ◽  
Vol 5 (5) ◽  
pp. 128-137
Author(s):  
Mohammed A Hussein ◽  
Raghad M Mahmmed ◽  
Afnan A Sebawaih ◽  
Basma A El-Maghraby ◽  
Eman E Mohammed ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hela Cells ◽  
Caspase 3 ◽  
Chitosan Nanoparticles ◽  
Induced Apoptosis

scholarly journals Autophagy inhibition enhances vorinostat-induced apoptosis via ubiquitinated protein accumulation

2009 ◽  
Vol 14 (10) ◽  
pp. 2448-2459 ◽  
Author(s):  
Jennifer S. Carew ◽  
Ernest C. Medina ◽  
Juan A. Esquivel II ◽  
Devalingam Mahalingam ◽  
Ronan Swords ◽  
...  
Keyword(s):  
Protein Accumulation ◽  
Ubiquitinated Protein ◽  
Induced Apoptosis ◽  
Autophagy Inhibition

scholarly journals Chemopreventive Effect of β-Cryptoxanthin on Human Cervical Carcinoma (HeLa) Cells Is Modulated through Oxidative Stress-Induced Apoptosis

Antioxidants ◽  
2019 ◽  
Vol 9 (1) ◽  
pp. 28 ◽  
Author(s):  
Enkhtaivan Gansukh ◽  
Arti Nile ◽  
Iyyakkannu Sivanesan ◽  
Kannan R. R. Rengasamy ◽  
Doo-Hwan Kim ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Cervical Carcinoma ◽  
Hela Cells ◽  
Caspase 3 ◽  
Nuclear Condensation ◽  
Physiological Concentration ◽  
Human Cervical Carcinoma ◽  
Induced Apoptosis

The present study was aimed to assess cellular and molecular events involved in the chemopreventive activities of β-cryptoxanthin derived from mandarin oranges (Citrus unshiu Marc.) on human cervical carcinoma (HeLa) cells. In vitro experiments established that β-cryptoxanthin significantly inhibited the proliferation of HeLa cells with the IC50 value of 4.5 and 3.7 µM after 24 and 48 h of treatments, respectively. β-cryptoxanthin-treated HeLa cells exhibited enhanced levels of oxidative stress correlated with significant downregulation of anti-apoptotic Bcl-2, and upregulation of pro-apoptotic Bax mRNA expression. Moreover, β-cryptoxanthin triggered nuclear condensation and disruption of the integrity of the mitochondrial membrane, upregulated caspase-3, -7, and -9 mRNA, and enhanced activation of caspase-3 proteins, resulting in nuclei DNA damage and apoptosis of HeLa cells. Remarkably, TUNEL assay carried out to detect nuclei DNA damage showed 52% TUNEL-positive cells after treatment with a physiological concentration of β-cryptoxanthin (1.0 μM), which validates its potential as an anticancer drug of natural origin.

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 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.

Sign in / Sign up

Export Citation Format

Share Document