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Article Abstract
Today, acute kidney injury (AKI) caused by sepsis, with its high incidence and rising mortality, is becoming a global problem. Many previous studies have proved that NLRP3 is a critical role in NLRP3 inflammasome activation to regulate inflammatory responses in a variety of diseases including AKI. Our study is aimed to explore the role and upstream regulatory mechanism of NLRP3 in AKI. In this study, we demonstrated that LPS treatment induced the upregulation of NLRP3 in HK-2 cells. Functionally, NLRP3 knockdown inhibited cell apoptosis, inflammatory response and NLRP3 inflammasome activation. Mechanistically, OIP5-AS1 competitively bound with miR-186-5p to promote NLRP3 level, and further activate TLR4/NF-κB signaling. Additionally, OIP5-AS1 was negatively associated with miR-186-5p but positively correlated with NLRP3 in rat renal tissues. The rescue assays suggested that NLRP3 reversed the effects of silencing OIP5-AS1 on cell apoptosis and inflammatory response. At last, OIP5-AS1 aggravated renal injury and inflammation in vivo. All findings indicated that the OIP5-AS1 contributed to sepsis-induced AKI by promoting NLRP3 inflammasome activation via miR-186-5p/NLRP3 axis. OIP5-AS1 could serve as a potential diagnostic and therapeutic marker in sepsis-induced AKI.
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