Preclinical Research Center, Daegu Gyeongbuk Medical Innovation Foundation, Daegu 41061, Korea.
Gyeongnam Bio-Health Research Support Center, Gyeongnam Branch Institute, Korea Institute of Toxicology (KIT), 17 Jeigok-gil, Jinju 52834, Korea.
Molecules. 2022 Aug 16;27(16):5215. doi: 10.3390/molecules27165215.
Cadmium (Cd), a harmful heavy metal, can lead to various pulmonary diseases, including chronic obstructive pulmonary disease (COPD), by inducing cytotoxicity and disturbing redox homeostasis. The aim of the present study was to investigate Cd-mediated cytotoxicity using human lung fibroblasts and the therapeutic potential of 3,3'-diindolylmethane (DIM). Cadmium significantly reduced the cell viability of human embryonic lung (HEL299) cells accompanied by enhanced oxidative stress as evidenced by the increased expression of autophagy-related proteins such as LC3B and p62. However, treatment with DIM significantly suppressed autophagic cell death in Cd-induced HEL299 fibroblasts. In addition, DIM induced antioxidant enzyme activity and decreased intracellular reactive oxygen species (ROS) levels in Cd-damaged HEL299 cells. This study suggests that DIM effectively suppressed Cd-induced lung fibroblast cell death through the upregulation of antioxidant systems and represents a potential agent for the prevention of various diseases related to Cd exposure.
镉（Cd）是一种有害的重金属，可通过诱导细胞毒性和扰乱氧化还原稳态，导致各种肺部疾病，包括慢性阻塞性肺疾病（COPD）。本研究旨在使用人肺成纤维细胞研究镉介导的细胞毒性以及 3,3′-二吲哚甲烷（DIM）的治疗潜力。镉显著降低人胚肺（HEL299）细胞的活力，同时伴有氧化应激增强，自噬相关蛋白如 LC3B 和 p62 的表达增加。然而，DIM 处理可显著抑制 Cd 诱导的 HEL299 成纤维细胞中的自噬性细胞死亡。此外，DIM 可诱导抗氧化酶活性并降低 Cd 损伤的 HEL299 细胞内活性氧（ROS）水平。本研究表明，DIM 通过上调抗氧化系统有效抑制 Cd 诱导的肺成纤维细胞死亡，是预防与 Cd 暴露相关的各种疾病的潜在药物。
