时间标签：数据日期 2026-10-31 · 生成时间 2026-11-01 05:30（Asia/Shanghai）｜ 检索窗口 PubMed edat 2026/10/28–2026/10/31 ｜ 情报发生日期 2026-10-31
研究问题
However, whether kaempferol counteracts BaP-induced pulmonary fibrosis remains unknown.
方法
Three groups were included: a blank control group, a BaP-only group (1 µM BaP for 24 h), and a combination group (1 µM BaP for 24 h followed by 25 µM kaempferol for another 24 h).；Cells were lysed in RIPA buffer, and protein concentrations were determined using a BCA protein assay kit.；Cultured cells were fixed and stained using a senescence-associated β-galactosidase staining kit (Beyotime, China) according to the manufacturer’s instructions.；Statistical analyses were performed using GraphPad Prism 9.5.1.
核心结论
PubChem provided the molecular structure of BaP, and we employed four databases (ChEMBL, PharmMapper, SwissTargetPrediction, and SuperPred) for target prediction.；A significant correlation was observed between the module and IPF traits (P < 0.05, ).；KEGG enrichment analysis of the 704 genes revealed significant enrichment in the Rap1, Wnt, and Ras signaling pathways (). ‖ 结论：Based on these findings, we link the therapeutic effect of kaempferol on BaP-induced pulmonary fibrosis to BaP-induced Ras/COX-2-mediated cellular senescence.
局限
Future studies should address these limitations.
对本项目的价值
★☆☆☆☆ 细胞衰老清除/重编程是项目干预管线的核心支柱之一。
全文来源
PMC JATS 全文（正文 25,029 字符，已过标题/DOI 逐字归属校验）
原文题录
- 英文标题：Integrative network toxicology and pharmacology reveal that kaempferol alleviates BaP-triggered pulmonary fibrosis via suppressing Ras/COX-2-dependent cellular senescence.
- 期刊与标识：Front Pharmacol · PMID 42959050 · DOI 10.3389/fphar.2026.1963570
B 级证据分级：B 级（同行评议临床前研究，主要为动物模型）
本文核心结论来自动物模型或体外细胞学，属临床前证据，不能外推至人体。「延长健康寿命」「改善功能」等表述在小鼠中的意义，与人类临床结局之间仍有距离。
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