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Autophagy inhibition-enhanced assembly of the NLRP3 inflammasome is associated with cisplatin-induced acute injury to the liver and kidneys in rats

机译:NLRP3炎症组的自噬抑制增强组装与顺铂诱导的大鼠肝脏和肾的顺铂诱导的急性损伤有关

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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-1 beta 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.
机译:含有3(NLRP3)炎症组的核苷酸结合寡聚化结构域样受体家族,炎症反应在炎症反应中具有关键作用。 我们发现顺铂(7.5,15mg / kg,iv)可诱导大鼠肝脏和肾脏的急性损伤。 Western印迹和免疫组织化学分析表明,在顺铂暴露后,以剂量依赖性方式显着上调NLRP3,Caspase-1和白细胞介素-1β的表达。 自噬可以抑制NLRP3炎症的NLRP3表达和组装。 轻链3 II / I和P62的表达表明,在肝脏和肾脏损伤期间抑制自噬。 这些数据表明,顺铂可能通过抑制大鼠肝脏和肾脏的自噬激活NLRP3。

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