TY -的A2 -陈,杰盟——苏,李汉AU - Lin Ming-Tsan AU -叶,Sung-Ling盟——叶Chiu-Li PY - 2021 DA - 2021/03/30 TI -谷氨酰胺政府变弱肾脏炎症在肥胖小鼠脓毒症复杂与幼童腹壁薄弱SP - 5597118六世- 2021 AB -肥胖是一个著名的世界各地的公共卫生问题。脓毒症是一种致命的临床综合症,导致multiorgan失败。肥胖可能会加重炎症在败血症的病人。谷氨酰胺(GLN)是一种营养与免疫监管和消炎作用。由于脓毒症是一种常见的急性肾损伤(AKI)的因素,本研究调查的影响GLN管理sepsis-induced炎症和阿基在肥胖的老鼠。高脂肪饮食由60%的热量来自脂肪提供10周诱导肥胖的老鼠。然后,肥胖老鼠分为败血症与生理盐水(SS)或GLN (SG)组。盲肠的结扎和穿刺(CLP)进行生产败血症。SS组静脉注射生理盐水在SG集团管理GLN CLP后一个或两个剂量。肥胖小鼠脓毒症牺牲在12日24或48 h post-CLP。 Results revealed that sepsis resulted in upregulated high-mobility group box protein-1 pathway-associated gene expression in obese mice. Also, expressions of macrophage/neutrophil infiltration markers and inflammatory cytokines in kidneys were elevated. Obese mice treated with GLN after sepsis reversed the depletion of plasma GLN, reduced production of lipid peroxides, and downregulated macrophage/neutrophil infiltration and the inflammatory-associated pathway whereas tight junction gene expression increased in the kidneys. These findings suggest that intravenously administered GLN to obese mice after sepsis alleviated inflammation and attenuated AKI. This model may have clinical application to obese patients with a risk for infection in abdominal surgery. SN - 0962-9351 UR - https://doi.org/10.1155/2021/5597118 DO - 10.1155/2021/5597118 JF - Mediators of Inflammation PB - Hindawi KW - ER -