苦杏仁苷通过抑制 LPS 处理的 BEAS-2B 支气管上皮细胞上的 TLR4/NF-κB 信号通路来减弱气道上皮细胞凋亡、炎症和上皮-间质转化,International Archives of Allergy and Immunology

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苦杏仁苷通过抑制 LPS 处理的 BEAS-2B 支气管上皮细胞上的 TLR4/NF-κB 信号通路来减弱气道上皮细胞凋亡、炎症和上皮-间质转化
International Archives of Allergy and Immunology ( IF 2.5 ) Pub Date : 2021-08-24 , DOI: 10.1159/000514209
Zhenyang Si ₁ , Biao Zhang ₁

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背景：咳嗽变异性哮喘（CVA）是一种特殊类型的哮喘，仅表现为咳嗽。研究表明气道炎症与 CVA 发病机制有关。苦杏仁苷被发现具有抗炎潜力，而它如何影响 CVA 仍有待探索。方法：不同浓度的 LPS 和苦杏仁苷对 BEAS-2B 细胞的细胞毒性通过 Cell Counting Kit-8 测定确定。CVA 体外模型是通过 LPS 暴露于经过苦杏仁苷预处理的 BEAS-2B 细胞上建立的。通过流式细胞术测定细胞凋亡。通过 ELISA 和 qRT-PCR 测量 BEAS-2B 细胞中肿瘤坏死因子 (TNF)-α、白细胞介素 (IL)-6、IL-8 和粘蛋白 5AC (MUC5AC) 的产生。TLR4、E-钙粘蛋白、N-钙粘蛋白、α-平滑肌肌动蛋白 (SMA)、波形蛋白、磷酸化-p65 (p-p65)、p65、磷酸化-IκBα (p-IκBα) 和 IκBα 在 BEAS-2B 细胞中的表达通过 qRT-PCR 或蛋白质印迹测量。结果：LPS 和高浓度苦杏仁苷（超过 600 μg/mL）可降低 BEAS-2B 细胞毒性。暴露于 LPS 抑制毒性，增强细胞凋亡；并促进 TNF-α、IL-6、IL-8 和 MUC5AC 的产生，增加 N-Cadherin、α-SMA、波形蛋白、p-p65 和 p-IκBα 的水平，并降低 E-cadherin 的水平和 BEAS-2B 细胞中的 IκBα。苦杏仁苷预处理抵消了 LPS 对 BEAS-2B 细胞的影响。过表达 TLR4 逆转了暴露于 LPS 的 BEAS-2B 细胞中苦杏仁苷的作用。结论：苦杏仁苷通过抑制CVA中的TLR4/NF-κB信号通路减弱气道上皮细胞凋亡、炎症和上皮间质转化。
Int Arch 过敏免疫

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Amygdalin Attenuates Airway Epithelium Apoptosis, Inflammation, and Epithelial-Mesenchymal Transition through Restraining the TLR4/NF-κB Signaling Pathway on LPS-Treated BEAS-2B Bronchial Epithelial Cells

Background: Cough-variant asthma (CVA) is a special type of asthma, solely manifesting with coughing. Studies suggest that airway inflammation is associated with CVA pathogenesis. Amygdalin is found to have an anti-inflammatory potential, while how it affects CVA remains unexplored. Methods: Cytotoxicity delivered by various concentrations of LPS and amygdalin on BEAS-2B cells was determined by Cell Counting Kit-8 assay. CVA in vitro models were established via LPS exposure on BEAS-2B cells which underwent amygdalin pretreatment. Cell apoptosis was determined by flow cytometry. Production of tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-8, and mucin 5AC (MUC5AC) in BEAS-2B cells was measured by ELISA and qRT-PCR. Expressions of TLR4, E-cadherin, N-cadherin, α-smooth muscle actin (SMA), vimentin, phosphorylated-p65 (p-p65), p65, phosphorylated-IκBα (p-IκBα), and IκBα in BEAS-2B cells were measured by qRT-PCR or Western blot. Results: LPS and high concentrations of amygdalin (over 600 μg/mL) decreased BEAS-2B cell toxicity. Exposure to LPS inhibited toxicity, enhanced apoptosis; and promoted production of TNF-α, IL-6, IL-8, and MUC5AC, increased the levels of N-Cadherin, α-SMA, vimentin, p-p65, and p-IκBα, and decreased the levels of E-cadherin and IκBα in BEAS-2B cells. Amygdalin pretreatment counteracted the effects of LPS on BEAS-2B cells. Overexpressing TLR4 reversed amygdalin-exerted effects in LPS-exposed BEAS-2B cells. Conclusion: Amygdalin attenuated airway epithelium apoptosis, inflammation and epithelial-mesenchymal transition through restraining the TLR4/NF-κB signaling pathway in CVA.
Int Arch Allergy Immunol

更新日期：2021-08-24

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