中国比较医学杂志2026，Vol.36Issue(8)：1-9,9.DOI:10.3969/j.issn.1671-7856.2026.08.001
香烟烟雾诱导的巨噬细胞条件培养基通过mTORC1/p70S6K通路促进气道上皮细胞炎症反应
Cigarette smoke-induced macrophage-conditioned medium triggers airway epithelial cell inflammatory responses through the mTORC1/p70S6K pathway
摘要
Abstract
Objective This study investigated the effects of cigarette smoke extract(CSE)-induced macrophage-conditioned medium on airway epithelial cells' inflammatory responses,and explored the underlying mechanisms involved.Methods Phorbol myristate acetate-induced differentiated monocytes and macrophages(THP-1)were cultured with 10％CSE for 24 h;the conditioned medium was collected to induce inflammatory responses in human bronchial epithelial cells(BEAS-2B).The effects of THP-1-conditioned medium on BEAS-2B cells viability were detected using the CCK-8 assay.The effects of conditioned medium on mRNA expression levels of inflammation-related factors in BEAS-2B cells were analyzed by RT-qPCR,and inflammatory cytokine secretion was measured with enzyme-linked immunosorbent assay.The effects of conditioned medium on BEAS-2B cells morphology were observed with immunofluorescence staining.The expression of proteins related to the mTOR/p70S6K pathway was examined by Western blot.Results BEAS-2B cells viability after treatment with 6.25％,12.5％,or 25％conditioned medium showed no significant changes after 6,12,24,or 48 h,while 50％,75％,and 100％induced significant reductions in cell viability(P＜0.05,P＜0.01).Conditioned medium at 6.25％,12.5％,and 25％significantly increased the mRNA expression and secretion of inflammatory factors interleukin(IL)-1β,IL-6,IL-8,and TNF-α in BEAS-2B cells(P＜0.05,P＜0.01),but had no significant effect on morphology.Levels of p-mTOR,p-p70S6K,p-GSK3β(Tyr216),and p-NF-KB p65 were significantly increased in conditioned medium-treated cells(P＜0.05,P＜0.01);the mTORC1 inhibitor rapamycin significantly reduced inflammatory factor mRNA expression in BEAS-2B cells induced by 25％conditioned medium.Conclusions CSE-induced macrophage-conditioned medium significantly induced airway epithelial cell inflammatory responses through activating the mTORC1/p70S6K pathway.关键词
慢性阻塞性肺疾病/炎症反应/气道上皮细胞/巨噬细胞/mTORC1/p70S6K通路Key words
chronic obstructive pulmonary disease/inflammatory response/airway epithelial cells/macrophages/mTORC1/p70S6K pathway分类
医药卫生引用本文复制引用
宋雨薇,王茜茜,杨博斐,秦燕勤..香烟烟雾诱导的巨噬细胞条件培养基通过mTORC1/p70S6K通路促进气道上皮细胞炎症反应[J].中国比较医学杂志,2026,36(8):1-9,9.基金项目
国家自然科学基金项目(82104662) （82104662）
河南省自然科学基金项目(252300420126) （252300420126）
中华中医药学会青年人才托举工程项目(CACM-2024-QNRC2-B35) （CACM-2024-QNRC2-B35）
河南省科技攻关计划项目(222102310141). （222102310141）
