Lin Ta-Chin, Lu Chia-Wen, Chang Kai-Fu, Lee Chung-Jen
Department of Surgery, National Defense Medical Center Tri-Service General Hospital Penghu Branch Magong City Taiwan.
Department of Nursing Buddhist Tzu Chi General Hospital Hualien Taiwan.
Food Sci Nutr. 2022 Jul 2;10(10):3405-3414. doi: 10.1002/fsn3.2941. eCollection 2022 Oct.
Septic shock can aggravate organ dysfunction and even lead to death. (JCo) extract has been experimentally demonstrated to have anti-inflammatory and antioxidant effects. We investigated the anti-inflammatory and antioxidant mechanism of JCo extract in vivo and in vitro. In a lipopolysaccharide (LPS)-induced acute kidney injury rat model, JCo extract improved animal survival, reduced kidney injury scores, suppressed kidney injury molecule-1, and preserved E-cadherin expression from LPS damage, as demonstrated by the immunohistochemistry examinations of the rat kidneys. In LPS-stimulated NRK-52E cells, JCo extract inhibited nuclear factor-κB (NF-κB) and increased adenosine monophosphate-activated protein kinase (AMPK) expression, prompting the activation of the antioxidant nuclear factor erythroid 2-related factor-2/heme oxygenase-1 pathway against oxidative stress. JCo extract ameliorated LPS-induced acute kidney injury by suppressing NF-κB signaling and stimulating the release of tumor necrosis factor-α and interleukin-1β through the AMPK pathway.
脓毒性休克会加重器官功能障碍，甚至导致死亡。（JCo）提取物已在实验中被证明具有抗炎和抗氧化作用。我们研究了JCo提取物在体内和体外的抗炎和抗氧化机制。在脂多糖（LPS）诱导的急性肾损伤大鼠模型中，JCo提取物提高了动物存活率，降低了肾损伤评分，抑制了肾损伤分子-1，并通过大鼠肾脏的免疫组织化学检查证明其保护了E-钙黏蛋白表达免受LPS损伤。在LPS刺激的NRK-52E细胞中，JCo提取物抑制核因子-κB（NF-κB）并增加腺苷单磷酸激活蛋白激酶（AMPK）表达，促使抗氧化核因子红细胞2相关因子-2/血红素加氧酶-1途径激活以对抗氧化应激。JCo提取物通过抑制NF-κB信号传导并通过AMPK途径刺激肿瘤坏死因子-α和白细胞介素-1β的释放，改善了LPS诱导的急性肾损伤。
