Chlorpyrifos (CPF) is a highly toxic commonly used pesticide and can seriously harm human health. This study assessed the potential of galangin (GAL), an antioxidant flavonoid, to attenuate oxidative stress, inflammation and kidney injury caused by CPF, emphasizing the role of farnesoid-x-receptor (FXR) and Nrf2. Rats were supplemented with CPF and GAL for 28 days. CPF increased serum creatinine, urea and Kim-1, provoked several tissue alterations, and increased kidney ROS, malondialdehyde (MDA), NF-κB p65, TNF-α, iNOS, and caspase-3. GAL effectively ameliorated serum kidney injury markers, ROS, MDA, and TNF-α, suppressed NF-κB p65, iNOS, and caspase-3, and enhanced antioxidants. GAL suppressed Keap1 and upregulated FXR, Nrf2, HO-1 and NQO-1 in CPF-administered rats. GAL exhibited binding affinity with Keap1, FXR, caspase-3, iNOS, HO-1, and NF-κB. In conclusion, GAL is effective in preventing CPF nephrotoxicity by attenuating oxidative stress and inflammation. This protection is linked to upregulation of antioxidants, Nrf2/HO-1 signaling and FXR.

中文翻译：

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高良姜素通过减轻氧化应激和炎症以及上调 Nrf2 和法尼酯 X 受体来减轻毒死蜱诱导的肾损伤


毒死蜱（CPF）是一种剧毒常用农药，严重危害人体健康。本研究评估了高良姜素 (GAL)（一种抗氧化剂黄酮类化合物）减轻 CPF 引起的氧化应激、炎症和肾损伤的潜力，强调了法尼醇 x 受体 (FXR) 和 Nrf2 的作用。给大鼠补充 CPF 和 GAL 28 天。 CPF 增加血清肌酐、尿素和 Kim-1，引发多种组织改变，并增加肾脏 ROS、丙二醛 (MDA)、NF-κB p65、TNF-α、iNOS 和 caspase-3。 GAL 可有效改善血清肾损伤标志物 ROS、MDA 和 TNF-α，抑制 NF-κB p65、iNOS 和 caspase-3，并增强抗氧化剂。在 CPF 给药的大鼠中，GAL 抑制 Keap1 并上调 FXR、Nrf2、HO-1 和 NQO-1。 GAL 表现出与 Keap1、FXR、caspase-3、iNOS、HO-1 和 NF-κB 的结合亲和力。总之，GAL 可通过减轻氧化应激和炎症来有效预防 CPF 肾毒性。这种保护与抗氧化剂、Nrf2/HO-1 信号传导和 FXR 的上调有关。