Abstract：
BACKGROUND: Ginkgo biloba leaf and seed have been traditionally used in ancient China for the treatment of cough and asthma. However, there is limited literature available on the anti-COPD effects and mechanisms of Ginkgo biloba.
OBJECTIVE: The aim of this study was to comprehensively investigate the therapeutic potential of ginkgo extracts in COPD through a combination of in vivo and in vitro functional experiments. Transcriptomic analyses were also employed to uncover novel molecular mechanisms underlying the therapeutic effects of ginkgetin in COPD.
METHODS: The therapeutic efficacy of ginkgo extracts was assessed in a COPD model. The anti-inflammatory effects of ginkgetin and its underlying molecular mechanisms were examined in A549 cells treated with cigarette smoke extract (CSE). Additionally, transcriptomic analyses were conducted to identify novel molecular pathways influenced by ginkgetin. These findings were further validated using quantitative real-time polymerase chain reaction (qPCR) and Western blot techniques.
RESULTS: The ethyl acetate extract of Ginkgo biloba L. seeds and ginkgetin treatment significantly reduced cytokine production in COPD mice. Following drug administration, lung function improved in different groups. The transcriptome data strongly supports the inhibitory effect of ginkgetin on CSE-induced inflammation through the downregulation of the c/EBPβ signaling pathway and subsequent inhibition of CCL2 expression.
CONCLUSIONS: Our results demonstrate that ginkgetin, one of the biflavones found in Ginkgo biloba, exhibits inhibitory effects on smoke-induced airway inflammation. This effect is achieved through the downregulation of the c/EBPβ signaling pathway and the reduction of CCL2 expression.
OBJECTIVE: The aim of this study was to comprehensively investigate the therapeutic potential of ginkgo extracts in COPD through a combination of in vivo and in vitro functional experiments. Transcriptomic analyses were also employed to uncover novel molecular mechanisms underlying the therapeutic effects of ginkgetin in COPD.
METHODS: The therapeutic efficacy of ginkgo extracts was assessed in a COPD model. The anti-inflammatory effects of ginkgetin and its underlying molecular mechanisms were examined in A549 cells treated with cigarette smoke extract (CSE). Additionally, transcriptomic analyses were conducted to identify novel molecular pathways influenced by ginkgetin. These findings were further validated using quantitative real-time polymerase chain reaction (qPCR) and Western blot techniques.
RESULTS: The ethyl acetate extract of Ginkgo biloba L. seeds and ginkgetin treatment significantly reduced cytokine production in COPD mice. Following drug administration, lung function improved in different groups. The transcriptome data strongly supports the inhibitory effect of ginkgetin on CSE-induced inflammation through the downregulation of the c/EBPβ signaling pathway and subsequent inhibition of CCL2 expression.
CONCLUSIONS: Our results demonstrate that ginkgetin, one of the biflavones found in Ginkgo biloba, exhibits inhibitory effects on smoke-induced airway inflammation. This effect is achieved through the downregulation of the c/EBPβ signaling pathway and the reduction of CCL2 expression.
摘要：
背景：银杏叶和种子在中国古代传统上用于治疗咳嗽和哮喘。然而,关于银杏叶的抗COPD作用和机制的文献有限。
目的：本研究的目的是通过体内和体外功能实验相结合，全面研究银杏提取物对COPD的治疗潜力。转录组学分析也被用来揭示银杏素治疗COPD的潜在分子机制。
方法：在COPD模型中评估银杏提取物的治疗效果。在用香烟烟雾提取物（CSE）处理的A549细胞中检查了银杏素的抗炎作用及其潜在的分子机制。此外,进行转录组学分析以鉴定受银杏素影响的新分子途径。使用定量实时聚合酶链反应(qPCR)和Western印迹技术进一步验证了这些发现。
结果：银杏叶种子的乙酸乙酯提取物和银杏素处理显著减少COPD小鼠的细胞因子产生。用药后,不同组肺功能改善。转录组数据强烈支持银杏素通过下调c/EBPβ信号通路和随后抑制CCL2表达对CSE诱导的炎症的抑制作用。
结论：我们的结果表明，银杏中发现的一种双黄酮，对烟雾诱导的气道炎症表现出抑制作用。这种作用是通过下调c/EBPβ信号通路和降低CCL2表达来实现的。
目的：本研究的目的是通过体内和体外功能实验相结合，全面研究银杏提取物对COPD的治疗潜力。转录组学分析也被用来揭示银杏素治疗COPD的潜在分子机制。
方法：在COPD模型中评估银杏提取物的治疗效果。在用香烟烟雾提取物（CSE）处理的A549细胞中检查了银杏素的抗炎作用及其潜在的分子机制。此外,进行转录组学分析以鉴定受银杏素影响的新分子途径。使用定量实时聚合酶链反应(qPCR)和Western印迹技术进一步验证了这些发现。
结果：银杏叶种子的乙酸乙酯提取物和银杏素处理显著减少COPD小鼠的细胞因子产生。用药后,不同组肺功能改善。转录组数据强烈支持银杏素通过下调c/EBPβ信号通路和随后抑制CCL2表达对CSE诱导的炎症的抑制作用。
结论：我们的结果表明，银杏中发现的一种双黄酮，对烟雾诱导的气道炎症表现出抑制作用。这种作用是通过下调c/EBPβ信号通路和降低CCL2表达来实现的。
