scholarly journals Altholactone induces reactive oxygen species-mediated apoptosis in bladder cancer T24 cells through mitochondrial dysfunction, MAPK-p38 activation and Akt suppression

2014 ◽  
Vol 31 (6) ◽  
pp. 2769-2775 ◽  
Author(s):  
BING ZHAO ◽  
XIAOMENG LI
Keyword(s):  
Reactive Oxygen Species ◽  
Bladder Cancer ◽  
Mitochondrial Dysfunction ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
T24 Cells

scholarly journals Bladder Cancer Chemosensitivity Is Affected by Paraoxonase-2 Expression

Antioxidants ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 175 ◽  
Author(s):  
Stefania Fumarola ◽  
Monia Cecati ◽  
Davide Sartini ◽  
Gianna Ferretti ◽  
Giulio Milanese ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Bladder Cancer ◽  
Caspase 3 ◽  
Reactive Oxygen ◽  
Caspase 8 ◽  
Activity Levels ◽  
Oxygen Species ◽  
T24 Cells ◽  
Before And After ◽  
And Migration

The goal of the current study was to identify potential roles of paraoxonase-2 in bladder carcinogenesis. T24 bladder cancer cells were transfected with plasmids inducing paraoxonase-2 silencing or overexpression. Upon the selection of clones stably down- or upregulating paraoxonase-2, cell proliferation, migration, and the production of reactive oxygen species were evaluated, before and after treatment with cisplatin and gemcitabine, used alone or in combination. The activity levels of both caspase-3 and caspase-8 were also analyzed. shRNA-mediated gene silencing and the overexpression of paraoxonase-2 revealed that the enzyme was able to promote both the proliferation and migration of T24 cells. Moreover, the knockdown of paraoxonase-2 was significantly associated with a reduced cell viability of T24 cells treated with chemotherapeutic drugs and led to both an increase of reactive oxygen species production and caspase-3 and caspase-8 activation. Conversely, under treatment with anti-neoplastic compounds, a higher proliferative capacity was found in T24 cells overexpressing paraoxonase-2 compared with controls. In addition, upon enzyme upregulation, both the production of reactive oxygen species and activation of caspase-3 and caspase-8 were reduced. Although further analyses will be required to fully understand the involvement of paraoxonase-2 in bladder tumorigenesis and in mechanisms leading to the development of chemoresistance, the data reported in this study seem to demonstrate that the enzyme could exert a great impact on tumor progression and susceptibility to chemotherapy, thus suggesting paraoxonase-2 as a novel and interesting molecular target for effective bladder cancer treatment.

scholarly journals Compound K Induces Apoptosis of Bladder Cancer T24 Cells Via Reactive Oxygen Species-Mediated p38 MAPK Pathway

2013 ◽  
Vol 28 (8) ◽  
pp. 607-614 ◽  
Author(s):  
Han Wang ◽  
Dandan Jiang ◽  
Jing Liu ◽  
Shuhong Ye ◽  
Shan Xiao ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Bladder Cancer ◽  
P38 Mapk ◽  
Mapk Pathway ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Compound K ◽  
T24 Cells ◽  
P38 Mapk Pathway

Butin reduces oxidative stress-induced mitochondrial dysfunction via scavenging of reactive oxygen species

2010 ◽  
Vol 48 (3) ◽  
pp. 922-927 ◽  
Author(s):  
Rui Zhang ◽  
Kyoung Ah Kang ◽  
Mei Jing Piao ◽  
Weon Young Chang ◽  
Young Hee Maeng ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Mitochondrial Dysfunction ◽  
Reactive Oxygen ◽  
Oxygen Species

scholarly journals Danshenol A Alleviates Hypertension-Induced Cardiac Remodeling by Ameliorating Mitochondrial Dysfunction and Suppressing Reactive Oxygen Species Production

2019 ◽  
Vol 2019 ◽  
pp. 1-18
Author(s):  
Kai Chen ◽  
Yiqing Guan ◽  
Yunci Ma ◽  
Dongling Quan ◽  
Jingru Zhang ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Mitochondrial Dysfunction ◽  
Cardiac Remodeling ◽  
Cardiac Fibrosis ◽  
Spontaneously Hypertensive Rat ◽  
Cardiac Injury ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Spontaneously Hypertensive ◽  
Underlying Mechanisms

Current therapeutic approaches have a limited effect on cardiac remodeling, which is characteristic of cardiac fibrosis and myocardial hypertrophy. In this study, we examined whether Danshenol A (DA), an active ingredient extracted from the traditional Chinese medicine Radix Salviae, can attenuate cardiac remodeling and clarified the underlying mechanisms. Using the spontaneously hypertensive rat (SHR) as a cardiac remodeling model, DA ameliorated blood pressure, cardiac injury, and myocardial collagen volume and improved cardiac function. Bioinformatics analysis revealed that DA might attenuate cardiac remodeling through modulating mitochondrial dysfunction and reactive oxygen species. DA repaired the structure/function of the mitochondria, alleviated oxidative stress in the myocardium, and restored apoptosis of cardiomyocytes induced by angiotensin II. Besides, DA inhibited mitochondrial redox signaling pathways in both the myocardium and cardiomyocytes. Thus, our study suggested that DA attenuates cardiac remodeling induced by hypertension through modulating mitochondrial dysfunction and reactive oxygen species.

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