scholarly journals Piscidin-1 Induces Apoptosis via Mitochondrial Reactive Oxygen Species-Regulated Mitochondrial Dysfunction in Human Osteosarcoma Cells

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Meng-Hsuan Cheng ◽  
Chieh-Yu Pan ◽  
Nan-Fu Chen ◽  
San-Nan Yang ◽  
Shuchen Hsieh ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Mitochondrial Dysfunction ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Mitochondrial Reactive Oxygen Species ◽  
Osteosarcoma Cells ◽  
Human Osteosarcoma ◽  
Human Osteosarcoma Cells

scholarly journals Phyllanthus urinariaInduces Apoptosis in Human Osteosarcoma 143B Cells via Activation of Fas/FasL- and Mitochondria-Mediated Pathways

2012 ◽  
Vol 2012 ◽  
pp. 1-13 ◽  
Author(s):  
Hsin-Yi Wu ◽  
Tsu-Kung Lin ◽  
Hsiao-Mei Kuo ◽  
Ya-Ling Huang ◽  
Chia-Wei Liou ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Mitochondrial Reactive Oxygen Species ◽  
Extrinsic Pathway ◽  
Membrane Potential Change ◽  
Therapeutic Modalities ◽  
Human Osteosarcoma ◽  
Human Osteosarcoma Cells ◽  
Ligand Expression

Phyllanthus urinaria (P. urinaria), in this study, was used for the treatment of human osteosarcoma cells, which is one of the tough malignancies with few therapeutic modalities. Herein, we demonstrated thatP. urinariainhibited human osteosarcoma 143B cells growth through an apoptotic extrinsic pathway to activate Fas receptor/ligand expression. Both intracellular and mitochondrial reactive oxygen species were increased to lead to alterations of mitochondrial membrane permeability and Bcl-2 family including upregulation of Bid, tBid, and Bax and downregulation of Bcl-2.P. urinariatriggered an intrinsic pathway and amplified the caspase cascade to induce apoptosis of 143B cells. However, upregulation of both intracellular and mitochondrial reactive oxygen species and the sequential membrane potential change were less pronounced in the mitochondrial respiratory-defective 143Bρ0cells compared with the 143B cells. This study offers the evidence that mitochondria are essential for the anticancer mechanism induced byP. urinariathrough both extrinsic and intrinsic pathways.

Sono-synthesis approach improves anticancer activity of ZnO nanoparticles: reactive oxygen species depletion for killing human osteosarcoma cells

Nanomedicine ◽  
2021 ◽  
Vol 16 (8) ◽  
pp. 657-671
Author(s):  
Mansoureh Parsa ◽  
Mohammad H Entezari ◽  
Azadeh Meshkini
Keyword(s):  
Reactive Oxygen Species ◽  
Anticancer Activity ◽  
Zno Nanoparticles ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Zno Nps ◽  
Human Osteosarcoma ◽  
Human Osteosarcoma Cells ◽  
Tumor Selectivity ◽  
Biological Tests

Aim: To investigate the effect of ultrasound during the synthesis of ZnO nanoparticles (NPs) on their anticancer activity. Materials & methods: ZnO NPs were synthesized in the presence and absence of ultrasonic irradiation. Biological tests were performed on human osteosarcoma cancer cells (Saos-2). Results: The sono-synthesized sample indicated higher cytotoxicity than the conventional one. (IC50 = 16.48 ± 0.41 μg/ml for sonochemical ZnO; 26.96 ± 0.33 μg/ml for conventional ZnO). Both sonochemical and conventional samples acted like antioxidants and reduced intracellular reactive oxygen species level. This reduction was more significant in cells treated with the sono-synthesized sample. The sono-synthesized ZnO NPs showed more tumor selectivity than the conventional sample. Conclusion: Sono-synthesis of ZnO NPs by a bath sonicator could improve their anticancer activity.

scholarly journals The synthetic antimicrobial peptide 19-2.5 attenuates mitochondrial dysfunction in cardiomyocytes stimulated with human sepsis serum

2016 ◽  
Vol 22 (8) ◽  
pp. 612-619 ◽  
Author(s):  
Lukas Martin ◽  
Carsten Peters ◽  
Lena Heinbockel ◽  
Julia Moellmann ◽  
Antons Martincuks ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Septic Shock ◽  
Antimicrobial Peptide ◽  
Mitochondrial Dysfunction ◽  
Reactive Oxygen ◽  
Septic Cardiomyopathy ◽  
Oxygen Species ◽  
Mitochondrial Reactive Oxygen Species ◽  
Mitochondrial Energy Metabolism ◽  
Ppar Γ

Septic cardiomyopathy affects up to 70% of patients with septic shock and the derangement of cardiac mitochondrial function contributes to the likelihood of death. However, at present, there is no specific therapeutic drug available. The peroxisome proliferator-activated receptor (PPAR)-γ coactivator-1α (PGC-1α) and coactivator-1β (PGC-1β) modulate members of the PPARs, which regulate mitochondrial energy metabolism and the production of mitochondrial reactive oxygen species in the heart. This study investigated the potential of the newly developed synthetic antimicrobial peptide 19-2.5 (Pep2.5) to attenuate mitochondrial dysfunction in murine cardiomyocytes stimulated with serum from septic shock patients. Pep2.5 treatment attenuated the suppression of PPAR-α, PPAR-γ ( P = 0.0004 and P = 0.0001, respectively) and PGC-1α/β ( P = 0.0008 and P = 0.0147, respectively) in cardiomyocytes stimulated with serum from septic shock patients compared with untreated cells. Pep2.5 treatment enhanced the mitochondrial maximum respiration ( P < 0.0001), increased cellular ATP levels ( P < 0.0001) and reduced the production of mitochondrial reactive oxygen species. Thus, the administration of Pep2.5 may have the potential as a promising therapeutic approach in septic cardiomyopathy by attenuating mitochondrial dysfunction in the septic heart.

scholarly journals Deoxyelephantopin Induces Reactive Oxygen Species-Mediated Apoptosis and Autophagy in Human Osteosarcoma Cells

2017 ◽  
Vol 42 (5) ◽  
pp. 1812-1821 ◽  
Author(s):  
Jilong Zou ◽  
Yan Zhang ◽  
Jiabing Sun ◽  
Xiaoyan Wang ◽  
Hualei Tu ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Viability ◽  
Morphological Changes ◽  
Reactive Oxygen ◽  
Annexin V ◽  
Underlying Mechanism ◽  
Ros Generation ◽  
Oxygen Species ◽  
Osteosarcoma Cells ◽  
Human Osteosarcoma Cells

Background/Aims: Osteosarcoma is the predominant form of primary bone malignancy. Although the combinational application of neoadjuvant chemotherapy and surgical resection significantly increases the survival rate, the therapeutic outcome remains unsatisfactory. Deoxyelephantopin (DET), an active ingredient of Elephantopus scaber, has been reported to have an anti-tumor effect in recent publications. This study aimed to investigate whether DET has antineoplastic effects on osteosarcoma cells and its underlying mechanism. Methods: Cell viability and morphological changes were assessed by MTT and Live/dead assays. Cell apoptosis, reactive oxygen species (ROS) and mitochondrial membrane potential were detected utilizing Annexin V-FITC/PI double staining, DCFH-DA and JC-1 probes, respectively. Autophagy was detected by mRFP-GFP-LC3 adenovirus transfection and western blot. Results: DET dose-dependently reduced the viability of osteosarcoma cells following the increase in intracellular ROS levels. Pretreatment with N-acetylcysteine (NAC) reversed this effect. Furthermore, DET induced mitochondrial apoptosis. Depolarized cells were increased, and apoptosis-related proteins, such as Bax, Bcl-2, cleaved caspase-9, cleaved caspase-3 and cleaved ploy ADP-ribose polymerase, were activated. Additionally, we found that DET could induce autophagy in osteosarcoma cells, but autophagy inhibition did not affect the decrease in cell viability. Conclusion: DET induced apoptosis in osteosarcoma cells through ROS generation, mitochondrial dysfunction and caspase activation; in addition, autophagy was involved in the effects of DET on osteosarcoma cells.

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