聚乙烯微塑料通过TLR4/NOX2轴诱导氧化应激,促进细胞衰老
Weilin Zhang1, Zhencong Li1, Zhongwei Wang1
1Department of Spinal Degeneration and Deformity Surgery, Affiliated Hospital of Guangdong Medical University, Zhanjiang 524001, China.
Ecotoxicology and environmental safety
|February 28, 2025
概括
微塑料存在于人类的椎间盘中,通过增加细胞衰老而导致退化. 聚乙烯微塑料激活了托尔类受体4 (TLR4) /NADPH氧化酶2 (NOX2) 途径,导致氧化应激和磁盘分解.
科学领域:
- 环境健康 环境健康
- 生物医学工程 生物医学工程
- 细胞生物学 细胞生物学
背景情况:
- 微塑料污染是一个日益严重的全球性问题.
- 微塑料对人体内部组织的存在和影响,如椎间盘,仍然在很大程度上未被探索.
- 椎间盘退化是背部疼痛和残疾的主要原因.
研究的目的:
- 检测和描述人类椎间盘组织中的微塑料.
- 研究聚乙烯微塑料 (PE-MPs) 对椎间盘变性产生的影响和分子机制.
- 探索微塑料诱导的磁盘退化潜在的治疗点.
主要方法:
- 拉曼光谱法用于识别和描述80个椎间盘样本中的微塑料.
- 建立了小鼠和核脉动细胞模型来研究PE-MPs的影响.
- 使用免疫光染色,CCK-8测定,西部涂抹和抑制剂治疗来评估氧化应激,细胞活力和分子通路.
主要成果:
- 在分析的椎间盘样本中有47%检测到微塑料,聚乙烯是最常见的类型.
- 暴露于PE-MPs诱导了细胞衰老和椎间盘退化.
- PE-MPs引发了氧化应激,并激活了托尔类受体4 (TLR4) /NADPH氧化酶2 (NOX2) 信号通路.
结论:
- 这项研究提供了人类椎间盘组织中微塑料的第一个证据.
- PE-MPs通过氧化应激和TLR4/NOX2轴诱导细胞衰老和椎间盘退化.
- 准TLR4/NOX2通路为微塑料诱导的磁盘退化提供了潜在的治疗策略.
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