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Resveratrol protects human bronchial epithelial cells against nickel‐induced toxicity via suppressing p38 MAPK, NF‐κB signaling, and NLRP3 inflammasome activation
Environmental Toxicology ( IF 4.4 ) Pub Date : 2020-05-01 , DOI: 10.1002/tox.22896 Xiangyu Cao 1 , Siqi Tian 1 , Mingyang Fu 1 , Yanmei Li 2 , Yueling Sun 3 , Jianli Liu 1 , Yue Liu 1
Environmental Toxicology ( IF 4.4 ) Pub Date : 2020-05-01 , DOI: 10.1002/tox.22896 Xiangyu Cao 1 , Siqi Tian 1 , Mingyang Fu 1 , Yanmei Li 2 , Yueling Sun 3 , Jianli Liu 1 , Yue Liu 1
Affiliation
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Nickel is a common environmental pollutant that can impair the lung, but the underlying mechanisms have not yet been fully elucidated. Furthermore, natural products are generally used to inhibit cell damage induced by heavy metal. Resveratrol possesses wide biological activities, including anti‐inflammation and antioxidative stress. This study was conducted to explore the toxicity of nickel on human bronchial epithelial (BEAS‐2B) cells and evaluate the protective effect of resveratrol. The results showed that nickel could induce cell apoptosis, increase oxidative stress, and promote the expression of pro‐inflammatory cytokines, including tumor necrosis factor‐α, interleukin (IL)‐1β, IL‐6, IL‐8, C‐reaction protein. Western blot analysis showed that nickel activated p38 mitogen‐activated protein kinase (MAPK), nuclear factor‐kappa B, and nucleotide‐binding oligomerization domain‐like receptor pyrin‐domain‐containing protein 3 pathways, while resveratrol could reverse these effects. Our results suggested that resveratrol could protect BEAS‐2B cells from nickel‐induced cytotoxicity. Therefore, resveratrol is a potential chemopreventive agent against nickel‐induced lung disease.
中文翻译：
白藜芦醇通过抑制 p38 MAPK、NF-κB 信号传导和 NLRP3 炎症小体激活保护人支气管上皮细胞免受镍诱导的毒性
镍是一种常见的环境污染物，会损害肺部，但其潜在机制尚未完全阐明。此外，天然产物通常用于抑制重金属诱导的细胞损伤。白藜芦醇具有广泛的生物活性，包括抗炎和抗氧化应激。本研究旨在探讨镍对人支气管上皮 (BEAS-2B) 细胞的毒性并评估白藜芦醇的保护作用。结果表明，镍可诱导细胞凋亡，增加氧化应激，促进促炎细胞因子的表达，包括肿瘤坏死因子-α、白细胞介素（IL）-1β、IL-6、IL-8、C-反应蛋白. 蛋白质印迹分析显示镍激活 p38 丝裂原活化蛋白激酶 (MAPK)、核因子-κB、和核苷酸结合寡聚化结构域样受体含有吡喃结构域的蛋白 3 通路，而白藜芦醇可以逆转这些影响。我们的结果表明，白藜芦醇可以保护 BEAS-2B 细胞免受镍诱导的细胞毒性。因此，白藜芦醇是一种潜在的化学预防剂，可预防镍诱发的肺病。
更新日期：2020-05-01
中文翻译：
白藜芦醇通过抑制 p38 MAPK、NF-κB 信号传导和 NLRP3 炎症小体激活保护人支气管上皮细胞免受镍诱导的毒性
镍是一种常见的环境污染物，会损害肺部，但其潜在机制尚未完全阐明。此外，天然产物通常用于抑制重金属诱导的细胞损伤。白藜芦醇具有广泛的生物活性，包括抗炎和抗氧化应激。本研究旨在探讨镍对人支气管上皮 (BEAS-2B) 细胞的毒性并评估白藜芦醇的保护作用。结果表明，镍可诱导细胞凋亡，增加氧化应激，促进促炎细胞因子的表达，包括肿瘤坏死因子-α、白细胞介素（IL）-1β、IL-6、IL-8、C-反应蛋白. 蛋白质印迹分析显示镍激活 p38 丝裂原活化蛋白激酶 (MAPK)、核因子-κB、和核苷酸结合寡聚化结构域样受体含有吡喃结构域的蛋白 3 通路，而白藜芦醇可以逆转这些影响。我们的结果表明，白藜芦醇可以保护 BEAS-2B 细胞免受镍诱导的细胞毒性。因此，白藜芦醇是一种潜在的化学预防剂，可预防镍诱发的肺病。
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