时间标签：数据日期 2026-11-03 · 生成时间 2026-11-03 05:30（Asia/Shanghai）｜ 检索窗口 PubMed edat 2026/10/31 – 2026/11/03 ｜ 情报发生日期 2026-11-03
证据级别：摘要级。本条依据 PubMed 结构化摘要与元数据撰写，付费墙全文未获取、未逐节核验，本站未做任何数值推算补全。
摘要（PubMed 原文节选）
Tributyl phosphate (TBP), a widely used organophosphate ester, exhibits lipophilic characteristics that enable it to cross the blood-brain barrier. Although its neurotoxicity has been confirmed, the underlying molecular pathways remain unclear. This study examined whether TLR4-associated autophagy disruption contributes to TBP-induced neuronal damage. Autophagy was activated with rapamycin (RAPA) and TLR4 was knocked down using siRNA. TBP exposure upregulated TLR4 expression and downregulated autophagy-related markers. Autophagic flux analysis assays using bafilomycin A1 further revealed that TBP impaired autophagosome biogenesis instead of lysosomal dysfunction. Autophagy activation and TLR…
对本项目的价值
中等价值：属「营养感知—自噬—蛋白稳态轴」方向；mTOR / 自噬 / 蛋白质稳态栏目可用作本项目文献库与综述素材。 ｜ 价值分 2.2/5（★★☆☆☆）
全文不可及原因
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原文题录
- 中文题名：磷酸三丁酯破坏神经元自噬：细胞与大鼠模型中 TLR4 的可能参与
- 英文标题：Tributyl phosphate disrupts neuronal autophagy: potential involvement of TLR4 in cell and rat models.
- 期刊与标识：Chem Biol Interact · PMID 42966556 · DOI 10.1016/j.cbi.2026.112403 · EDAT 2026-10-31