Cigarette smoke induces the pyroptosis of urothelial cells through ROS/NLRP3/caspase‐1 signaling pathway

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.

Roles of Inflammasome in Cigarette Smoke-Related Diseases and Physiopathological Disorders: Mechanisms and Therapeutic Opportunities

“…Two recent researches concentrated on the change of inflammasome in cigarette smoke-related urinary diseases, including kidney injury and bladder dysfunction (43,44). Zheng et al (43) proposed that nicotine induced NLRP6 inflammasome activation via alpha7 nicotinic acetylcholine receptor in human kidney cells and mouse kidney tissue.…”

“…Zheng et al (43) proposed that nicotine induced NLRP6 inflammasome activation via alpha7 nicotinic acetylcholine receptor in human kidney cells and mouse kidney tissue. Besides, Wu et al (44) found that cigarette smoke induced the pyroptosis of urothelial cells through ROS/NLRP3/caspase-1 signaling pathway in bladder dysfunction models.…”

“…In clinical practice, NAC has been used as a mucolytic to help clear mucus in patients with respiratory diseases (61). Several studies verified that NAC could decrease ROS generation and further inhibit NLRP3 inflammasome activation, and NAC-mediated disease/disorder involved atherosclerosis (41), bladder damage (44), and podocyte injury (46). Besides NAC, other therapies antagonizing ROS were also explored to modulate inflammasome activation in cigarette smoke-induced diseases.…”

Overexpressed LncRNA ADAMTS9-AS2 inhibited gastric cancer (GC) development and sensitized chemoresistant GC cells to cisplatin by regulating miR-223-3p/NLRP3 axis

“…The specimens from tissues and cells were lysed by the lysis buffer. The contents of total proteins were evaluated by Bradford method and a microplate reader was employed to examine the optical density (OD) values at the wavelength of 405 nm, which was utilized to represent caspase-1 activity according to the previous study [38].…”

“…Briefly, the GC cells were administered with different treatments, and the supernants were harvested. The LDH reagent was used to detect LDH release at the wavelength of 490 nm according to the previous study [38].…”