| 熊贵鑫,张彦,孟万里,等.海洋苔藓虫中全新小分子C2抗急性肺损伤的活性及机制研究[J].中国海洋药物,2025,44(6):27-34. |
| 海洋苔藓虫中全新小分子C2抗急性肺损伤的活性及机制研究 |
| Study on the anti-acute lung injury activity and mechanism of novel small molecules from Marine bryozoans |
| 投稿时间：2024-05-07 修订日期：2024-05-13 |
| DOI：10.13400/j.cnki.cjmd.2025.06.003 |
| 中文关键词: 急性肺损伤 海洋天然小分子 抗炎活性 信号通路 |
| English Keywords:Acute lung injury Marine natural small molecules Anti-inflammatory activity Signaling pathways |
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| 中文摘要: |
| 目的 探究海洋小分子化合物C2对脂多糖诱导大鼠急性肺损伤的作用及机制。方法 70只大鼠按体重随机分为5组：对照组、脂多糖(lipopolysaccharide, LPS)模型组、阳性药地塞米松(dexamethasone, DEX)组、化合物C2低、高剂量组(25 mg/kg、50 mg/kg)。采用气管滴注法构建脂多糖诱导的大鼠急性肺损伤模型,检测C2对大鼠肺组织干湿重比、髓过氧化物酶水平的变化；检测对大鼠血清和肺泡灌洗液中炎症因子TNF-α、IL-1β和IL-6水平的变化；血液分析仪检测对大鼠肺泡灌洗液中炎症细胞的影响。采用H&E染色检测大鼠肺脏的组织病理学情况。通过Western blotting技术检测炎症相关信号通路IκB、p-NF-κB和p-MAPK蛋白的表达水平。结果 C2可以降低肺组织的水肿程度及肺组织中髓过氧化物酶的水平；可以降低肺泡灌洗液中白细胞总数及中性粒细胞、淋巴细胞、单核细胞和嗜酸性粒细胞数量；可以降低肺泡灌洗液和血清中炎症因子TNF-α、IL-1β和IL-6水平；H&E染色显示C2可以缓解肺泡组织破坏、肺间质增厚和炎症浸润程度；Western blotting 结果表明C2可以调节炎症相关信号通路IκB和p-NF-κB蛋白的表达水平。结论 化合物C2可以改善LPS诱导的大鼠急性肺损伤,作用机制可能与其抑制NF-κB p65信号通路，降低炎症细胞数量，下调炎症因子水平有关。 |
| English Summary: |
| Objective To investigate the effect and mechanism of Marine small molecular compound C2 on LPS-induced acute lung injury in rats. Methods Seventy rats were randomly divided into 5 groups according to body weight: control group, lipopolysaccharide (LPS) model group, dexamethasone (DEX) group, compound C2 low and high dose (25 mg/kg, 50 mg/kg) groups. Acute lung injury model was established induced by lipopolysaccharide using tracheal instillation method. The changes of dry to wet weight ratio of lung tissue and myeloperoxidase level were detected. The levels of TNF-α, IL-1β and IL-6 in serum and bronchoalveolar lavage fluid (BALF) were detected. Using blood analyzer to detect the number of inflammatory cells in BALF. H E staining was used to detect the histopathology damage. Western blotting was used to detect the protein expression levels of IκB, p-NF-κB and p-MAPK. Results C2 can reduce the degree of lung edema and the level of myeloperoxidase in lung tissue, reduce the total number of white blood cells, neutrophils, lymphocytes, monocytes and eosinophils in BALF. The results of Elisa showed that, C2 can reduce the levels of TNF-α, IL-1β and IL-6 in BALF and serum. HE staining showed that, C2 can alleviate alveolar tissue destruction, pulmonary interstitial thickening and inflammatory infiltration. The results of Western blotting showed that C2 can regulate the expression levels of IκB and p-NF-κB proteins. Conclusion Compound C2 can improve LPS-induced acute lung injury in rats, and its mechanism may be related to inhibiting the NF-κB p65 signaling pathways, and reducing the number of inflammatory cells, down-regulating the levels of inflammatory factors. |
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