| 李君明,盛燚,洪志星,詹玉飞.虫草素对脂多糖诱导的急性肺损伤大鼠的保护作用及TLR4/NF-κB通路的影响[J].浙江中西医结合杂志,2022,32(11): |
| 虫草素对脂多糖诱导的急性肺损伤大鼠的保护作用及TLR4/NF-κB通路的影响 |
| Protective effect of cordycepin on lipopolysaccharide induced acute lung injury in rats and Influence of TLR4/NF-κB pathway |
| 投稿时间：2022-01-10 修订日期：2022-10-20 |
| DOI： |
| 中文关键词: 虫草素 急性肺损伤 炎症反应 Toll样受体4/核因子-κB通路 |
| 英文关键词:cordycepin acute lung injury inflammatory reaction toll like receptor 4/nuclear factor-κB pathway |
| 基金项目: |
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| 中文摘要: |
| 目的：探讨虫草素对脂多糖诱导的急性肺损伤（ALI）大鼠的保护作用及Toll样受体4（TLR4）/核因子-κB（NF-κB）通路的影响。方法：通过脂多糖诱导建立ALI大鼠模型，造模48只大鼠随机分成：模型组、虫草素低（5 mg/kg）、中（10 mg/kg）、高（20 mg/kg）剂量组，12只/组；另设12只健康大鼠作为对照组。虫草素各剂量组大鼠腹腔注射相应剂量的虫草素，模型组和对照组大鼠腹腔注射等量生理盐水，连续给药1周（1次/d）。检测大鼠动脉血氧分压（PaO2）、二氧化碳分压（PaCO2）、肺组织肿瘤坏死因子-α（TNF-α）、白细胞介素-6（IL-6）、白细胞介素-1β（IL-1β）、TLR4、NF-κB信使核糖核酸（mRNA）和蛋白水平，观察肺组织形态学并进行肺损伤评分。结果：对照组大鼠肺泡组织结构正常；模型组肺泡组织受损，毛细血管扩张，红细胞渗漏和肺组织液分泌，可见炎症细胞浸润；虫草素干预后，肺泡组织趋于正常，肺泡壁变薄，红细胞、分泌液减少，炎症细胞浸润减少。与对照组比较，模型组大鼠PaO2水平降低，PaCO2、肺损伤评分、肺组织TNF-α、IL-6、IL-1β、TLR4、NF-κB mRNA和蛋白水平升高（P<0.05）；与模型组比较，虫草素低、中、高剂量组大鼠PaO2水平依次升高，PaCO2、肺损伤评分、肺组织TNF-α、IL-6、IL-1β、TLR4、NF-κB mRNA和蛋白水平依次降低（P<0.05）。结论：虫草素可改善ALI大鼠肺功能和肺损伤，降低肺部炎症反应，其机制可能与虫草素抑制ALI大鼠肺组织TLR4、NF-κB mRNA和蛋白表达进而抑制TLR4/NF-κB通路的激活有关。 |
| 英文摘要: |
| Objective: To investigate the protective effect of cordycepin on lipopolysaccharide induced acute lung injury (ALI) in rats and toll like receptor 4 (TLR4) / nuclear factor-κB (NF-κB) Impact of access. Methods: ALI rat model was established by lipopolysaccharide induction. 48 model rats were randomly divided into model group, cordycepin low (5 mg/kg), medium (10 mg/kg), high (20 mg/kg) dose group, 12 rats/group; Another 12 healthy rats were used as the control group. Rats in each dose group of cordycepin were intraperitoneally injected with corresponding doses of cordycepin, and rats in model group and control group were intraperitoneally injected with the same amount of normal saline, continuous administration for 1 week (once a day). Arterial partial pressure of oxygen (PaO2), partial pressure of carbon dioxide (PaCO2), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), interleukin-1 β (IL-1β), TLR4, NF-κB messenger RNA (mRNA) and protein levels in lung tissue were measured. Lung histomorphology was observed and lung injury score was performed. Results: The alveolar structure of the control group was normal; in the model group, alveolar tissue was damaged, capillaries dilated, red blood cell leakage and lung tissue fluid secretion, and inflammatory cell infiltration was observed; after cordycepin intervention, alveolar tissue tended to be normal, alveolar wall became thinner, red blood cells and secretory fluid decreased, and inflammatory cell infiltration decreased. Compared with the control group, the level of PaO2 in the model group was decreased, PaCO2, lung injury score and the levels of TNF-α, IL-6, IL-1β, TLR4, NF-κB mRNA and protein in lung tissue were increased (P<0.05); compared with the model group, the PaO2 levels of rats in cordycepin low, medium and high dose groups were increased in turn, PaCO2, lung injury score and the levels of TNF-α, IL-6, IL-1β, TLR4, NF-κB mRNA and protein in lung tissue were decreased in turn (P<0.05). Conclusion: Cordycepin can improve lung function, lung injury and reduce lung inflammatory response in ALI rats, its mechanism may be related to cordycepin inhibiting the expression of TLR4, NF-κB mRNA and protein in lung tissue of ALI rats, and then inhibiting the activation of TLR4/NF-κB pathway. |
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