Polybrominated diphenyl ethers quinone exhibits neurotoxicity by inducing DNA damage, cell cycle arrest, apoptosis and p53-driven adaptive response in microglia BV2 cells

Toxicology ◽  
2021 ◽  
pp. 152807
Author(s):  
Zixuan Liu ◽  
Qiushuang Zhu ◽  
Erqun Song ◽  
Yang Song
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Cell Cycle Arrest ◽  
Polybrominated Diphenyl Ethers ◽  
Adaptive Response ◽  
Damage Cell ◽  
Cycle Arrest ◽  
Bv2 Cells ◽  
Diphenyl Ethers

Cr(VI) Induces DNA Damage, Cell Cycle Arrest and Polyploidization: A Flow Cytometric and Comet Assay Study inPisum sativum

2011 ◽  
Vol 24 (7) ◽  
pp. 1040-1047 ◽  
Author(s):  
Eleazar Rodriguez ◽  
Raquel Azevedo ◽  
Pedro Fernandes ◽  
Conceic¸ão Santos
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Comet Assay ◽  
Cell Cycle Arrest ◽  
Damage Cell ◽  
Cycle Arrest ◽  
Flow Cytometric

Celastrol Induced DNA Damage, Cell Cycle Arrest, and Apoptosis in Human Rheumatoid Fibroblast-Like Synovial Cells

2013 ◽  
Vol 41 (03) ◽  
pp. 615-628 ◽  
Author(s):  
Zengtao Xu ◽  
Guosheng Wu ◽  
Xu Wei ◽  
Xiuping Chen ◽  
Yitao Wang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Cell Cycle Arrest ◽  
Inflammatory Diseases ◽  
Annexin V ◽  
Synovial Fibroblasts ◽  
Damage Cell ◽  
Cycle Arrest ◽  
M Phase

Celastrol is one of the principal active ingredients of Tripterygium wilfordii Hook.f., a toxic Chinese medical herb traditionally prescribed for controlling pain and inhibiting inflammation in various chronic inflammatory diseases, including rheumatoid arthritis (RA). Resistance to apoptosis of fibroblast-like synoviocytes is considered a major characteristic of RA. In this study, we test celastrol's cytotoxic effect and potential mechanisms in human rheumatoid synovial fibroblasts (RA-FLS). In the cytotoxic assay, we found that celastrol dose-dependently decreased RA-FLS viability and increased LDH release. The apoptotic nuclear morphology was observed after celastrol treatment as determined by DAPI fluorescence staining. Flow cytometry analysis with PI and Annexin V revealed that celastrol induced RA-FLS cell cycle arrest in the G2/M phase and apoptosis. Furthermore, celastrol dramatically increased expression of Bax/Bcl-2, proteolytic cleavage of Caspase-3, -9, PARP, and decreased expression of FasR. In addition, celastrol treatment resulted in DNA damage. Collectively, we concluded that celastrol inhibits RA-FLS proliferation by inducing DNA damage, cell cycle arrest, and apoptosis in vitro, which might provide data for its application in RA treatment.

scholarly journals Antiproliferative activity of goniothalamin enantiomers involves DNA damage, cell cycle arrest and apoptosis induction in MCF-7 and HB4a cells

2015 ◽  
Vol 30 (1) ◽  
pp. 250-263 ◽  
Author(s):  
Simone Cristine Semprebon ◽  
Lilian Areal Marques ◽  
Gláucia Fernanda Rocha D'Epiro ◽  
Elaine Aparecida de Camargo ◽  
Glenda Nicioli da Silva ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Cell Cycle Arrest ◽  
Antiproliferative Activity ◽  
Apoptosis Induction ◽  
Damage Cell ◽  
Cycle Arrest ◽  
Mcf 7

Differences in the Induction of DNA Damage, Cell Cycle Arrest, and Cell Death by 5-Fluorouracil and Antifolates

2001 ◽  
Vol 12 (5) ◽  
pp. 231-239 ◽  
Author(s):  
H.H.J. Backus ◽  
H.M. Pinedo ◽  
D. Wouters ◽  
C.M. Kuiper ◽  
G. Jansen ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Cell Death ◽  
Cell Cycle Arrest ◽  
Damage Cell ◽  
Cycle Arrest
Sign in / Sign up

Export Citation Format

Share Document