Abstract Bisphenol A (BisPH-A) is a latent danger that threatens our health, which we frequently exposure in our modern life (e.g. the widespread use of drinking water in plastic pet bottles). But the BisPH-A induced transient receptor potential melastatin 2 (TRPM2)-mediated oxidative stress and apoptosis in these cells has not been studied yet. Calcium (Ca2+) plays an important role in a versatile intracellular signal transduction that works over a wide range to regulate oxidative stress processes. TRPM2 is activated by oxidative stress and it has emerged as an important Ca2+ signaling mechanism in a variety of cells, contributing many cellular functions including cell death. Resveratrol (RESV), which belongs to the polyphenol group, acts as an antioxidant, eliminating cellular oxidative stress and increasing the body’s resistance to diseases. The current study aimed to elucidate the effect of antioxidant resveratrol on TRPM2-mediated oxidative stress induced by BisPH-A exposure in the mouse kidney cortical collecting duct cells (mpkCCDcl4). The cells were divided into four groups as control, resveratrol (50 µM for 24 h), BisPH-A (100 µM for 24 h) and BisPH-A + RESV. Intracellular free Ca2+ concentrations and TRPM2 channel currents were high in BisPH-A treated cells, but decreased with resveratrol treatment. In addition, BisPH-A induced mitochondrial membrane depolarization, reactive oxygen species (ROS), caspase 3, caspase 9 and apoptosis values were decreased by the resveratrol treatment. In conclusion, resveratrol protected cells from BisPH-A induced oxidative damage. In this study, we showed that TRPM2 channel mediates this protective effect of resveratrol.

中文翻译：

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白藜芦醇通过小鼠肾皮质集合管细胞中的 TRPM2 通道减少双酚 A 诱导的氧化应激

摘要 双酚 A (BisPH-A) 是威胁我们健康的潜在危险，我们在现代生活中经常接触到它（例如广泛使用塑料宠物瓶中的饮用水）。但是尚未研究 BisPH-A 在这些细胞中诱导的瞬时受体电位 melastatin 2 (TRPM2) 介导的氧化应激和细胞凋亡。钙 (Ca2+) 在多功能细胞内信号转导中发挥重要作用，可在广泛的范围内调节氧化应激过程。TRPM2 被氧化应激激活，它已成为多种细胞中重要的 Ca2+ 信号传导机制，有助于许多细胞功能，包括细胞死亡。白藜芦醇 (RESV) 属于多酚类，可作为抗氧化剂，消除细胞氧化应激，增加人体对疾病的抵抗力。目前的研究旨在阐明抗氧化剂白藜芦醇对小鼠肾皮质集合管细胞 (mpkCCDcl4) 中 BisPH-A 暴露诱导的 TRPM2 介导的氧化应激的影响。将细胞分为四组作为对照、白藜芦醇（50 µM，24 小时）、BisPH-A（100 µM，24 小时）和 BisPH-A + RESV。在 BisPH-A 处理的细胞中，细胞内游离 Ca2+ 浓度和 TRPM2 通道电流很高，但随着白藜芦醇处理而降低。此外，BisPH-A 诱导的线粒体膜去极化、活性氧 (ROS)、caspase 3、caspase 9 和细胞凋亡值通过白藜芦醇处理降低。总之，白藜芦醇保护细胞免受 BisPH-A 诱导的氧化损伤。在这项研究中，我们表明 TRPM2 通道介导了白藜芦醇的这种保护作用。