| 李涛,丛明慧,孙静,等.海洋来源小分子CH103抗PM2.5诱导肺损伤的作用研究[J].中国海洋药物,2024,43(5):28-36. |
| 海洋来源小分子CH103抗PM2.5诱导肺损伤的作用研究 |
| Protective effects of alkaloid compound CH103 on PM2.5 induced lung damage and dysfunction |
| 投稿时间：2024-07-15 修订日期：2024-08-04 |
| DOI：10.13400/j.cnki.cjmd.2024.05.006 |
| 中文关键词: 海洋来源小分子 氧化应激 肺腔灌洗液 炎症因子 肺泡 |
| English Keywords:marine alkaloid compounds oxidative stress pulmonary lavage fluid inflammatory factors lung alveolar |
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| 中文摘要: |
| 目的 PM2.5是当今社会环境中可诱导肺癌、慢阻肺等呼吸系统疾病的高危因素,从海洋中挖掘可防治PM2.5对肺部损伤的天然物质具有重要价值。本文研究了海洋来源天然生物碱类小分子CH103抗PM2.5诱导肺上皮细胞氧化应激和小鼠肺组织炎症损伤的治疗作用及其药理机制。方法 首先建立一定浓度PM2.5诱导II型肺泡上皮细胞A549氧化应激模型,通过MTT、Western Blotting等方法检测不同浓度CH103对肺上皮细胞的保护和抗氧化应激的作用机制。然后采用气道滴注PM2.5溶液构建肺部损伤的小鼠模型,通过血象分析仪检测小鼠肺泡灌洗液(BALF)中炎症细胞的数量,酶联免疫吸附法(ELISA)检测BALF上清中细胞因子的含量,通过H E染色方法对CH103改善PM2.5诱发肺损伤的药物效果进行评价。 结果 结果显示CH103能够有效抑制PM2.5诱导肺上皮细胞的活力下降和活性氧ROS产生,且具有毒性低的优点。同时,CH103显著降低PM2.5诱导肺上皮细胞p38MAPK和NF-κB的磷酸化,明显改善PM2.5诱导小鼠体质量降低的状况,有效减少小鼠BALF中的TNF-α、MCP-1和MMP-13、MMP-14等炎症因子以及炎症细胞的水平,并明显改善肺组织病理进展。这表明CH103能够通过p38MAPK和NF-κB信号通路遏制肺上皮细胞氧化损伤和小鼠肺组织炎症浸润、肺泡萎陷、结缔组织增生等病理损伤,可作为治疗肺损伤和预防肺癌性病变的候选化合物用于进一步研究。 |
| English Summary: |
| Objective To investigate the therapeutic effect of CH103 on PM2.5-induced pulmonary dysfunction in mice and cell models. Methods Firstly, the animal model of pulmonary dysfunction was established by instilling PM2.5 solution into the mice airway, then the Leukocyte (White blood cell) and lymphocytes number in bronchoalveolar lavage fluid (BALF) of mice was counted by hemogram analyzer, and the inflammatory cytokines in the supernatant of BALF was analyzed by ELISA assay. Secondly, phosphorylation levels of NF-κB and p38MAPK in A549 were measured by Western blotting. Then the effect of CH103 on pulmonary damage was evaluated by H E staining methods. Results The results showed that CH103 could significantly improve the lung dysfunction of mice, effectively reduce the contents of inflammatory cytokines such as, TNF-α, MCP-1, MMP-13 and MMP-14 in the supernatant of mice alveolar lavage fluid, and dramatically inhibit the levels of p38MAPK and NF-κB as well as ROS in lung epithelial cell A549. The inflammatory infiltration, alveolar atrophy, ECM deposition and blood vessel congestion in mice lung tissue were obviously improved. |
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