scholarly journals Genistein selectively potentiates arsenic trioxide‐induced apoptosis in human leukemia cellsviareactive oxygen species generation and activation of reactive oxygen species‐inducible protein kinases (p38‐MAPK, AMPK)

2008 ◽  
Vol 123 (5) ◽  
pp. 1205-1214 ◽  
Author(s):  
Yolanda Sánchez ◽  
Donna Amrán ◽  
Carlos Fernández ◽  
Elena de Blas ◽  
Patricio Aller
Keyword(s):  
Reactive Oxygen Species ◽  
Arsenic Trioxide ◽  
Protein Kinases ◽  
P38 Mapk ◽  
Reactive Oxygen ◽  
Human Leukemia ◽  
Oxygen Species ◽  
Inducible Protein ◽  
Induced Apoptosis

scholarly journals Inhibition of p38 MAPK sensitizes tumour cells to cisplatin‐induced apoptosis mediated by reactive oxygen species and JNK

2013 ◽  
Vol 5 (11) ◽  
pp. 1759-1774 ◽  
Author(s):  
Lorena Pereira ◽  
Ana Igea ◽  
Begoña Canovas ◽  
Ignacio Dolado ◽  
Angel R. Nebreda
Keyword(s):  
Reactive Oxygen Species ◽  
P38 Mapk ◽  
Reactive Oxygen ◽  
Tumour Cells ◽  
Oxygen Species ◽  
Induced Apoptosis

Reactive oxygen species mediation of Baizhu-induced apoptosis in human leukemia cells

2005 ◽  
Vol 97 (1) ◽  
pp. 21-29 ◽  
Author(s):  
Huey-Lan Huang ◽  
Chien-Chih Chen ◽  
Chin-Yi Yeh ◽  
Ray-Ling Huang
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Leukemia Cells ◽  
Human Leukemia ◽  
Oxygen Species ◽  
Human Leukemia Cells ◽  
Induced Apoptosis

scholarly journals Synergistic Apoptosis-Inducing Antileukemic Effects of Arsenic Trioxide andMucuna macrocarpaStem Extract in Human Leukemic Cells via a Reactive Oxygen Species-Dependent Mechanism

2012 ◽  
Vol 2012 ◽  
pp. 1-14 ◽  
Author(s):  
Kuan-Hung Lu ◽  
Hui-Ju Lee ◽  
Min-Li Huang ◽  
Shang-Chih Lai ◽  
Yu-Ling Ho ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Arsenic Trioxide ◽  
Reactive Oxygen ◽  
Butylated Hydroxytoluene ◽  
Leukemic Cells ◽  
Human Leukemia ◽  
Oxygen Species ◽  
Folk Remedy ◽  
Human Leukemic Cells ◽  
Dependent Mechanism

The objective of this study was to examine the potential of enhancing the antileukemic activity of arsenic trioxide (ATO) by combining it with a folk remedy, crude methanolic extract ofMucuna macrocarpa(CMEMM). Human leukemia cells HL-60, Jurkat, and Molt-3 were treated with various doses of ATO, CMEMM, and combinations thereof for 24 and 48 h. Results indicated that the combination of 2.5 μM ATO and 50 μg/mL CMEMM synergistically inhibited cell proliferation in HL-60 and Jurkat cell lines. Apoptosis triggered by ATO/CMEMM treatment was confirmed by accumulation of cells in the sub-G1phase in cell cycle analyses, characteristic apoptotic nuclear fragmentation, and increased percentage of annexin V-positive apoptotic cells. Such combination treatments also led to elevation of reactive oxygen species (ROS). The antioxidantsN-acetyl cysteine (NAC), butylated hydroxytoluene, andα-tocopherol prevented cells from ATO/CMEMM-induced apoptosis. The ATO/CMEMM-induced activation of caspase-3 and caspase-9 can be blocked by NAC. In summary, these results suggest that ATO/CMEMM combination treatment exerts synergistic apoptosis-inducing effects in human leukemic cells through a ROS-dependent mechanism and may provide a promising antileukemic approach in the future.

scholarly journals Ang (1–7) Protects Islet Endothelial Cells from Palmitate-Induced Apoptosis by AKT, eNOS, p38 MAPK, and JNK Pathways

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Li Yuan ◽  
Chun-Li Lu ◽  
Ying Wang ◽  
Yang Li ◽  
Xiao-Ya Li
Keyword(s):  
Reactive Oxygen Species ◽  
Endothelial Cells ◽  
P38 Mapk ◽  
Reactive Oxygen ◽  
Treated Group ◽  
Ros Production ◽  
Oxygen Species ◽  
Concomitant Reduction ◽  
Jnk Inhibitors ◽  
Induced Apoptosis

This study aimed to explore the effect of angiotensin (1–7) (Ang (1–7)) on palmitate-induced apoptosis in islet endothelial cells and the mechanism of action. MS-1 cells were treated with palmitate in the presence or absence of Ang (1–7). The percentage of apoptotic cells was determined by DNA fragmentation and flow cytometry. Reactive oxygen species (ROS) production was measured using a Reactive Oxygen Species Assay Kit. Expression of AKT, eNOS, C-Jun N-terminal kinase (JNK), and p38 was detected by western blotting. Compared with palmitate treated group, palmitate-induced apoptosis was decreased in MS-1 cells which were preincubated with Ang (1–7) (P<0.05). Palmitate decreased the phosphorylation of AKT and eNOS, and Ang (1–7) increased the phosphorylation of these kinases (P<0.05), with a concomitant reduction in MS-1 cells apoptosis. Ang (1–7) also inhibited the palmitate-induced ROS production and attenuated the apoptosis-related signaling molecule JNK and p38 activation (allP<0.05). PI3K/AKT, eNOS, p38 MAPK, and JNK inhibitors blocked the antilipoapoptosis of Ang (1–7) (allP<0.05). Our findings suggest that Ang (1–7) reduces palmitate-induced islet endothelial cells apoptosis. AKT/eNOS/NO signaling and JNK and p38 pathway are involved in the Ang (1–7)-mediated modulation of islet endothelial cells lipoapoptosis.

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