Phytol shows anti-angiogenic activity and induces apoptosis in A549 cells by depolarizing the mitochondrial membrane potential

2018 ◽  
Vol 105 ◽  
pp. 742-752 ◽  
Author(s):  
Ravi Sakthivel ◽  
Dicson Sheeja Malar ◽  
Kasi Pandima Devi
Keyword(s):  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
A549 Cells ◽  
Angiogenic Activity

Glutamine protects mitochondrial structure and function in oxygen toxicity

2001 ◽  
Vol 280 (4) ◽  
pp. L779-L791 ◽  
Author(s):  
Shama Ahmad ◽  
Carl W. White ◽  
Ling-Yi Chang ◽  
Barbara K. Schneider ◽  
Corrie B. Allen
Keyword(s):  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Tricarboxylic Acid Cycle ◽  
A549 Cells ◽  
Oxygen Toxicity ◽  
Cycle Enzyme ◽  
Glutamine Deprivation ◽  
And Function ◽  
Dose Dependent Increase

Glutamine is an important mitochondrial substrate implicated in the protection of cells from oxidant injury, but the mechanisms of its action are incompletely understood. Human pulmonary epithelial-like (A549) cells were exposed to 95% O2 for 4 days in the absence and presence of glutamine. Cell proliferation in normoxia was dependent on glutamine, and glutamine deprivation markedly accelerated cell death in hyperoxia. Glutamine significantly increased cellular ATP levels in normoxia and prevented the loss of ATP in hyperoxia seen in glutamine-deprived cells. Mitochondrial membrane potential as assessed by flow cytometry with chloromethyltetramethylrosamine was increased by glutamine in hyperoxia-exposed A549 cells, and a glutamine dose-dependent increase in mitochondrial membrane potential was detected. Glutamine-supplemented, hyperoxia-exposed cells had a higher O2 consumption rate and GSH content. Electron and fluorescence microscopy revealed that, in hyperoxia, glutamine protected cellular structures, especially mitochondria, from damage. In hyperoxia, activity of the tricarboxylic acid cycle enzyme α-ketoglutarate dehydrogenase was partially protected by its indirect substrate, glutamine, indicating a mechanism of mitochondrial protection.

scholarly journals The Novel H7N9 Influenza A Virus NS1 Induces p53-Mediated Apoptosis of A549 Cells

2016 ◽  
Vol 38 (4) ◽  
pp. 1447-1458 ◽  
Author(s):  
Yinxia Yan ◽  
Yongming Du ◽  
Gefei Wang ◽  
Yuxue Deng ◽  
Rui Li ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Influenza A ◽  
Caspase 3 ◽  
Eastern China ◽  
A549 Cells ◽  
Epithelial Cell Line ◽  
Ns1 Protein ◽  
Protein Levels

Background: H7N9, emerged as an avian influenza virus outbreak in Eastern China in early 2013, and represented another major threat to global health. Roles of its NS1 protein, an essential viral factor, in regulating apoptosis remain unknown. Methods: Apoptotic effect and features of H7N9/NS1 in the human A549 alveolar basal epithelial cell line were examined by caspase 3/7 activity assay and western blotting of apoptotic associated proteins. Effects of H7N9/NS1on mitochondrial membrane potential were investigated by flow cytometry. Results: The expression of H7N9/NS1 in A549 cells activated caspase 3/7 and increased the protein levels of cleaved caspase 7 and cleaved poly (ADP-ribose) polymerase (PARP). H7N9/NS1-expressing A549 cells displayed a decrease in mitochondrial membrane potential. In addition, H7N9/NS1 increased the protein levels of total p53, p53 phosphorylated at Ser46 and Ser37, activated caspase 9, and the Bax/Bcl-2 ratio. Conclusion: Our results suggest that H7N9/NS1 protein causes the accumulation of p53 by increasing phosphorylation levels of p53 and the induction of mitochondrial dysfunction, which may contribute to H7N9/NS1-induced apoptosis in A549 cells.

scholarly journals Apoptotic effect of astaxanthin from white shrimp shells on lung cancer A549 cells

2020 ◽  
Vol 19 (9) ◽  
pp. 1835-1842
Author(s):  
Supita Tanasawet ◽  
Wanida Sukketsiri ◽  
Pennapa Chonpathompikunlert ◽  
Pennapa Chonpathompikunlert ◽  
Wanwimol Klaypradit ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Litopenaeus Vannamei ◽  
Mitochondrial Membrane ◽  
Caspase 3 ◽  
A549 Cells ◽  
Nuclear Staining ◽  
Dependent Manner

Purpose: To investigate the anti-cancer potential of astaxanthin from Litopenaeus vannamei encapsulated in liposomes (ASX) to treat lung cancer A549 cells.Methods: Lung adenocarcinoma A549 cells were cultured and treated with ASX, following which cell viability and nuclear staining were performed. Generation of ROS was identified by the DCFH-DA assay while tetramethylrhodamine ethyl ester was used to determine the mitochondrial membrane potential. Flow cytometry was applied to investigate caspase-3/7 activity and cell cycle distribution.Results: ASX inhibited growth of A549 in a concentration- and time- dependent manner. The IC50 values at 24, 48 and 72 h were 53.73, 22.85, 17.46 μg/mL, respectively (p < 0.05). After incubation with ASX, the morphological changes were observed in A549 cells following Hoechst 33342/PI fluorescent staining. ASX increased ROS generation and was associated with the collapse of mitochondrial membrane potential, which subsequently triggered the activation of caspase-3/7 activity leading to apoptosis (p < 0.05). In addition, A549 cells accumulated in the G0/G1 phase.Conclusion: The results suggest that ASX is a valuable nutraceutical agent to target A549 lung cancer cells via ROS-dependent pathway as well as blockage of cell cycle progression. Keywords: Astaxanthin, Litopenaeus vannamei, Lung cancer, A549, Apoptosis

scholarly journals Ophiopogonin B-inducing Pyroptosis Through Caspase-1/gsdmd Pathway Contributes to Alleviation of Paclitaxel Resistance in Lung Cancer Cells 

2020 ◽  
Author(s):  
Ziyu Cheng ◽  
Zhihui Li ◽  
Ling Gu ◽  
Liqiu Li ◽  
Qian Gao ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Drug Resistance ◽  
Membrane Potential ◽  
Cancer Cells ◽  
Mitochondrial Membrane Potential ◽  
Nude Mice ◽  
Release Rate ◽  
Mitochondrial Membrane ◽  
A549 Cells ◽  
Caspase 1

Abstract Background: Drug resistance has become the main reason for the failure of tumor chemotherapy. In our previous study, ophiopogonin B (OP-B) has been verified to inhibit cell proliferation in numerous non-small cell lung cancer (NSCLC) cells. However, it is still unknown whether it can improve the drug resistance of lung cancer cells. Herein, we compared the inhibition effects of OP-B on NCI-H460, A549, A549/DDP and A549/PTX cells, and tried to find out the most sensible cell line to OP-B and the underlying reasons. Methods: The sensitivity of NCI-H460, A549, A549/DDP, and A549/PTX cells to OP-B was determined by CCK-8 assay, and the results were further verified in orthotopic tumor nude mice model and zebrafish tumor model. To identify pyroptosis in the cells, electron microscopy was used to observe cell morphology, flow cytometry was used to detect the mitochondrial membrane potential, and the LDH release rate was analyzed by microplate reader. Otherwise, immunofluorescence and immunohistochemical staining assay, western blot and qRT-PCR were used for detection of pyroptosis-correlated pathway.Results: In vitro, A549/DDP cell was verified to be most sensitive to OP-B than NCI-H460, A549, or A549/PTX cells. In vivo, OP-B inhibited the growth of A549/DDP orthotopic tumor more significantly than that of A549 both in nude mice and zebrafish models. Cell morphological feature, mitochondrial membrane potential, LDH release rate, production of IL-1β and expression of Caspase-1/GSDMD all showed that pyroptosis happened more significantly in A549/DDP cells than that in A549 cells after OP-B treatment.Conclusion: Though inducing more significantly pyroptosis by activating Caspase-1/GSDMD pathway, OP-B relieved DDP resistance of A549 cells.

scholarly journals Potential Toxicity of Polymyxins in Human Lung Epithelial Cells

2017 ◽  
Vol 61 (6) ◽  
Author(s):  
Maizbha U. Ahmed ◽  
Tony Velkov ◽  
Yu-Wei Lin ◽  
Bo Yun ◽  
Cameron J. Nowell ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Human Lung ◽  
A549 Cells ◽  
Polymyxin B ◽  
Lung Epithelial Cells ◽  
Time Dependent ◽  
Gram Negative ◽  
Lung Epithelial

ABSTRACT Inhaled polymyxins are of considerable utility in achieving optimal exposure in the respiratory tract for the treatment of lung infections caused by multidrug-resistant Gram-negative pathogens. Current inhaled polymyxin therapy is empirical, and often large doses are used that may lead to potential pulmonary adverse effects. This study aimed to investigate the effect of polymyxins on human lung epithelial (A549) cells. The viability of A549 cells was examined after treatment with polymyxins by flow cytometry. Activation of caspases 3, 8, and 9, expression of Fas ligand (FasL), loss of mitochondrial membrane potential, and mitochondrial oxidative stress induced by polymyxin B were evaluated. The concentration of polymyxin B required to induce 50% of maximal cell death was 1.74 mM (95% confidence interval, 1.60 to 1.90 mM). Colistin was at least 2-fold less toxic than polymyxin B, while colistimethate was nontoxic. With 2.0 mM polymyxin B, 30.6% ± 11.5% (mean ± standard deviation) of the cells were apoptotic at 8 h and this increased to 71.3% ± 3.72% at 24 h. Concentration- and time-dependent activation of caspases 3, 8, and 9 was evident, while the activation of caspase 9 was more dramatic. Furthermore, polymyxin B caused concentration- and time-dependent FasL expression, production of mitochondrial reactive oxygen species, and changes in mitochondrial membrane potential. This is the first study to demonstrate that both extrinsic death receptor and intrinsic mitochondrial pathways are involved in polymyxin-induced toxicity in A549 cells. This knowledge base is critical for the development of novel strategies for the safe and effective inhalation therapy of polymyxins against Gram-negative “superbugs.”

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