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许夏燕,李智,潘明月,韩雨彤,易刚强,袁劲松.五甲基槲皮素改善香烟烟雾提取物诱导的急性加重慢性阻塞性肺疾病[J].湖南中医药大学学报英文版,2022,42(8):1283-1288.[Click to copy
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| 五甲基槲皮素改善香烟烟雾提取物诱导的急性加重慢性阻塞性肺疾病 |
| 许夏燕,李智,潘明月,韩雨彤,易刚强,袁劲松 |
| (汕头大学医学院, 广东 汕头 515041;深圳市罗湖区人民医院, 广东 深圳 518000;湖南中医药大学, 湖南 长沙 410208;汕头大学医学院, 广东 汕头 515041;北京大学深圳医院, 广东 深圳 518000) |
| 摘要: |
| 目的 探讨五甲基槲皮素对急性加重慢性阻塞性肺疾病（acute exacerbation of chronic obstructive pulmonary disease,AECOPD）的预防作用及相关机制。方法 采用香烟烟雾提取物刺激人支气管上皮BEAS-2B细胞，建立AECOPD细胞模型。采用不同浓度五甲基槲皮素干预AECOPD细胞模型，分为4组：对照组、五甲基槲皮素1 μmol/L组、五甲基槲皮素3 μmol/L组和五甲基槲皮素10 μmol/L组。干预结束后收集细胞蛋白及上清液。采用ELISA实验检测上清液中IL-6、IL-8的浓度；采用蛋白免疫印迹法检测各组样本中磷脂酰肌醇3-激酶（phosphatidylinositol 3-kinase,PI3K）、蛋白激酶B（proteinkinase B,AKT）、P38蛋白激酶（P38 mitogen-activated protein kinase,P38）、应激活化蛋白激酶（c-Jun N-terminal kinase,JNK）、B-细胞淋巴瘤因子2（B-cell lymphoma-2,BCL-2）、半胱氨酸蛋白酶3（Caspase 3）以及活化后半胱氨酸蛋白酶3（cleaved Caspase 3）的蛋白丰度。结果 五甲基槲皮素可剂量依赖性降低IL-6和IL-8的释放，与对照组相比，五甲基槲皮素3 μmol/L组和五甲基槲皮素10 μmol/L组对IL-6的释放抑制更为明显（P<0.01），五甲基槲皮素10 μmol/L组IL-8水平明显降低（P<0.01）；同时，五甲基槲皮素10 μmol/L组PI3K（P<0.01）、AKT（P<0.01）、P38（P<0.05）、JNK（P<0.05）、Caspase 3（P<0.01）以及cleaved Caspase 3（P<0.001）的蛋白水平降低，并且BCL-2的蛋白表达增加（P<0.01）。结论 五甲基槲皮素可通过PI3K/AKT、P38和JNK等信号通路改善AECOPD模型中细胞的炎性反应，同时可通过调节Caspase 3和BCL-2抑制细胞的凋亡，提示五甲基槲皮素具有预防AECOPD发生发展的潜在药理作用。 |
| 关键词: 急性加重慢性阻塞性肺疾病 五甲基槲皮素 炎性反应 凋亡 半胱氨酸蛋白酶3 B-细胞淋巴瘤因子2 磷脂酰肌醇3-激酶 蛋白激酶B |
| DOI：10.3969/j.issn.1674-070X.2022.08.010 |
| Received:March 30, 2022 |
| 基金项目:长沙市自然科学基金项目（kq2007040）；深圳市罗湖区软科学研究计划项目（LX20201101）。 |
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| Pentamethylquercetin ameliorates cigarette smoke extract induced acute exacerbation of chronic obstructive pulmonary disease |
| XU Xiayan,LI Zhi,PAN Mingyue,HAN Yutong,YI Gangqiang,Yuan Jingsong |
| (Shantou Medical University, Shantou, Guangdong 515041, China;Shenzhen Luohu District People's Hospital, Shenzhen, Guangdong 518000, China;Hunan University of Chiese Medicine, Changsha, Hunan 410208, China;Shantou Medical University, Shantou, Guangdong 515041, China;Shenzhen Hospital of Beijing University, Shenzhen, Guangdong 518000, China) |
| Abstract: |
| Objective To investigate the preventive effect of pentamethylquercetin on acute exacerbation of chronic obstructive pulmonary disease (AECOPD) and its related mechanism. Methods Cigarette smoke extract was used to stimulated human bronchial epithelial BEAS-2B cells to establish AECOPD cell model, and divided into 4 groups:control group, pentamethylquercetin 1 μmol/L group, pentamethylquercetin 3 μmol/L group and pentamethylquercetin 10 μmol/L group. Cell protein and supernatant were collected after intervention. The content of IL-6 and IL-8 in supernatant were detected by ELISA. The protein expression levels of phosphatidylinositol 3-kinase (PI3K), proteinkinase B (AKT), P38 mitogen-activated protein kinase (P38), c-Jun N-terminal kinase (JNK), B-cell lymphoma-2 (BCL-2), Caspase 3 and cleaved Caspase 3 were detected by Western blot. Results Pentamethylquercetin can reduce the release of IL-6 and IL-8 in a dose-dependent manner. Compared with control group, the release of IL-6 was significantly inhibited in pentamethylquercetin 3 μmol/L group and pentamethylquercetin 10 μmol/L group (P<0.01), and IL-8 level in pentame-thylquercetin 10 μmol/L group decreased (P<0.01). Meanwhile, pentamethylquercetin 10 μmol/L group decreased the expression of PI3K (P<0.01), AKT (P<0.01), P38 (P<0.05), JNK (P<0.05), Caspase 3 (P<0.01) and cleaved Caspase 3 (P<0.001), and increased BCL-2 protein level (P<0.01). Conclusion Pentamethylquercetin can improve the inflammatory reaction in AECOPD model via inhibiting PI3K/AKT, P38 and JNK pathway, and can inhibit cell apoptosis by modulating Caspase 3 and BCL-2, which indicated the potential pharmacological effect of pentamethylquercetin on AECOPD. |
| Key words: acute exacerbation of chronic obstructive pulmonary disease pentamethylquercetin inflammatory reaction apoptosis cleaved Caspase 3 B-cell lymphoma-2 phosphatidylinositol 3-kinase proteinkinase B |
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