TY -的A2 -莫拉莱斯,帕特丽夏盟——金正日Jung-Yeon盟——Leem Jaechan AU -香港,Hyo-Lim PY - 2021 DA - 2021/01/05 TI -蜂毒肽改善Endotoxin-Induced急性肾损伤通过抑制炎症,氧化应激,小鼠和细胞死亡SP - 8843051六世- 2021 AB - Sepsis-related急性肾损伤(AKI)是一个全球健康问题,及其发病机制涉及多个通路。脂多糖(LPS)是一种内毒素诱发系统性炎症反应。蜂毒肽,蜂毒的主要成分,对一些生物活性如抗氧化剂,抗炎,抗凋亡的行动。然而,是否蜂毒肽预防endotoxin-induced阿基仍未确定。这里,我们旨在研究蜂毒素的潜在行动LPS-induced肾损伤和探索的机制。我们表明,急性肾功能衰竭和结构损伤后注射LPS明显减毒蜂毒素的政府。肽也抑制表达标记LPS-treated直接管损伤肾脏的老鼠。从力学上看,蜂毒肽减少系统性和肾功能水平的细胞因子和抑制肾免疫细胞积累与伴随的抑制核转录因子kappa-B途径。有限合伙人治疗后增加大量的脂质过氧化反应产品在很大程度上减少了蜂毒肽。此外,肽的表达减少烟酰胺腺嘌呤二核苷酸磷酸氧化酶4和增强的核因子erythroid-2-related因子2-mediated抗氧化防御。 Moreover, melittin inhibited apoptotic and necroptotic cell death after LPS treatment. Lastly, we showed that melittin improved the survival rate of LPS-injected mice. These results suggest that melittin ameliorates endotoxin-induced AKI and mortality through inhibiting inflammation, oxidative injury, and apoptotic and necroptotic death of tubular epithelial cells. SN - 1942-0900 UR - https://doi.org/10.1155/2021/8843051 DO - 10.1155/2021/8843051 JF - Oxidative Medicine and Cellular Longevity PB - Hindawi KW - ER -