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- Title
Cigarette smoke induces the pyroptosis of urothelial cells through ROS/NLRP3/caspase‐1 signaling pathway.
- Authors
Wu, Zonglong; Liu, Qinggang; Zhu, Kejia; Liu, Yaxiao; Chen, Lipeng; Guo, Hongda; Zhou, Nan; Li, Yan; Shi, Benkang
- Abstract
Aims: Cell death and inflammation are involved in the development of bladder dysfunction. Pyroptosis is programmed cell death, causing cytotoxic effects and local inflammation. As one of the biggest health threats in the world, smoking is also closely related to urinary system diseases. The aims of this study were to investigate the role of NLRP3 inflammasome‐mediated pyroptosis in the bladder after cigarette smoke exposure. Methods: The expression of NLRP3 inflammasome and the activity of caspase‐1 in bladder tissue was investigated after cigarette smoke exposure. In vitro, bladder urothelial cells were stimulated by cigarette smoke extract and then the activity of caspase‐1 and the expression of NLRP3 inflammasome were measured. The role of oxidative stress was also assessed. Results: The activity of caspase‐1 in bladder tissue increased by 50% after cigarette smoke exposure. Cigarette smoke caused oxidative stress injury and the activation of NLRP3 inflammasome. In addition, reactive oxygen species (ROS) inhibitor N‐acetyl‐cysteine alleviated the pyroptosis of urothelial cells. Conclusions: Cigarette smoke‐induced pyroptosis of bladder tissue by activating ROS/NLRP3/caspase‐1 signaling pathway. Inhibition of bladder urothelial cell pyroptosis may be a new approach to alleviate bladder damage caused by smoking.
- Subjects
CIGARETTE smoke; NLRP3 protein; APOPTOSIS; CELL death; OXIDATIVE stress; REACTIVE oxygen species
- Publication
Neurourology & Urodynamics, 2020, Vol 39, Issue 2, p613
- ISSN
0733-2467
- Publication type
Article
- DOI
10.1002/nau.24271