Autophagy inhibition-enhanced assembly of the NLRP3 inflammasome is associated with cisplatin-induced acute injury to the liver and kidneys in rats.
Xiao-Yu QuHuan GaoLina TaoYueming ZhangJinghui ZhaiYanqing SongSixi ZhangPublished in: Journal of biochemical and molecular toxicology (2018)
The nucleotide-binding oligomerization domain-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome has a key role in the inflammatory response. We found that cisplatin (7.5, 15 mg/kg, IV) could induce acute injury to the liver and kidneys of rats. Western blot and immunohistochemical analyses showed that expression of NLRP3, caspase-1 and interleukin-1β was upregulated significantly in a dose-dependent manner after cisplatin exposure. Autophagy could inhibit NLRP3 expression and assembly of the NLRP3 inflammasome. Expression of light chain 3 II/I and p62 suggested that autophagy was inhibited during injury to the liver and kidneys. These data suggested that cisplatin might activate NLRP3 by inhibiting autophagy in the liver and kidneys of rats.
Keyphrases
- nlrp inflammasome
- cell death
- poor prognosis
- signaling pathway
- endoplasmic reticulum stress
- inflammatory response
- oxidative stress
- binding protein
- liver failure
- induced apoptosis
- long non coding rna
- drug induced
- south africa
- electronic health record
- machine learning
- big data
- hepatitis b virus
- toll like receptor
- transcription factor
- extracorporeal membrane oxygenation
- acute respiratory distress syndrome