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• W2903156966 abstract "The rapid production and release of a large number of inflammatory cytokines can cause excessive local and systemic inflammation in severe acute pancreatitis (SAP) and multiple organ dysfunction syndrome (MODS), especially pancreatitis-associated acute lung injury (P-ALI), which is the main cause of early death in patients with SAP. The NLRP3 inflammasome plays an important role in the maturation of IL-1 β and the inflammatory cascade. Here, we established a model of SAP using wild-type (NLRP3 +/+ ) and NLRP3 knockout (NLRP3 -/- ) mice by intraperitoneal injections of caerulein (Cae) and lipopolysaccharide (LPS). Pathological injury to the pancreas and lungs, the inflammatory response, and neutrophil infiltration were significantly mitigated in NLRP3 -/- mice. Furthermore, INF-39, an NLRP3 inflammasome inhibitor, could reduce the severity of SAP and P-ALI in a dose-dependent manner. Our results suggested that SAP and P-ALI were alleviated by NLRP3 deficiency in mice, and thus, reducing NLRP3 expression may mitigate SAP-associated inflammation and P-ALI." @default.
• W2903156966 created "2018-12-11" @default.
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• W2903156966 date "2018-11-28" @default.
• W2903156966 modified "2023-10-14" @default.
• W2903156966 title "NLRP3 Deficiency Alleviates Severe Acute Pancreatitis and Pancreatitis-Associated Lung Injury in a Mouse Model" @default.
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• W2903156966 doi "https://doi.org/10.1155/2018/1294951" @default.
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