TY -的A2, Young-Su盟——Tanuseputero莎朗安吉拉AU - Lin Ming-Tsan AU -叶,Sung-Ling盟——叶Chiu-Li PY - 2020 DA - 2020/05/11 TI -静脉精氨酸管理会使NLRP3 Inflammasome活动和减弱急性肾损伤在脓毒症小鼠幼童腹壁薄弱SP - 3201635六世- 2020 AB -急性肾损伤(AKI)是脓毒症的主要并发症。核苷结合域样受体蛋白3 (NLRP3)炎症小体是介导脓毒性AKI的多蛋白复合物。精氨酸(l -精氨酸)是分解代谢条件下的条件必需氨基酸，是一氧化氮(NO)生成的底物;然而，它在脓毒症的应用是有争议的。本研究探讨了静脉注射Arg对脓毒性AKI相关NLRP3炎症小体活性的调节作用。将小鼠分为正常对照组(NC)、假手术组(sham)、脓毒症盐水组(SS)和脓毒症免疫球蛋白组(SA)。为了研究NO的作用，我们在脓毒症组使用了诱导型NO合成酶抑制剂L-N6-(1-亚氨基乙基)-盐酸赖氨酸(L-NIL)。采用盲肠结扎和穿刺(CLP)诱导脓毒症。中耳炎后1 h, SS组和SA组经尾静脉给予生理盐水或Arg治疗。分别于脓毒症后6、12、24 h处死小鼠。 The results showed that compared to the NC group, septic mice had higher plasma kidney function parameters and lower Arg levels. Also, renal NLRP3 inflammasome protein expression and tubular injury score increased. After Arg treatment, plasma Arg and NO levels increased, kidney function improved, and expressions of renal NLRP3 inflammasome-related proteins were downregulated. Changes in plasma NO and renal NLRP3 inflammasome-related protein expression were abrogated when L-NIL was given to the Arg sepsis groups. Arg plus L-NIL administration also attenuated kidney injury after CLP. The findings suggest that intravenous Arg supplementation immediately after sepsis restores plasma Arg levels and is beneficial for attenuating septic AKI, partly via NO-mediated NLRP3 inflammasome inhibition. SN - 0962-9351 UR - https://doi.org/10.1155/2020/3201635 DO - 10.1155/2020/3201635 JF - Mediators of Inflammation PB - Hindawi KW - ER -