| 刘婷1，万芝灵1，刘舜星1，李慧1，林如涛1，黄垚1，单春兰1，缪福俊2.棕榈油酸对脂多糖诱导的小鼠急性肺损伤的保护作用[J].中国油脂,2025,50(10):.[LIU Ting1，WAN Zhiling1，LIU Shunxing1，LI Hui1，LIN Rutao1，
HUANG Yao1，SHAN Chunlan1 ，MIAO Fujun2.Protective effect of palmitoleic acid on acute lung injury induced by lipopolysaccharide in mice[J].China Oils and Fats,2025,50(10):.] |
| 棕榈油酸对脂多糖诱导的小鼠急性肺损伤的保护作用 |
| Protective effect of palmitoleic acid on acute lung injury induced by lipopolysaccharide in mice |
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出版日期：
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| DOI：10.19902/j.cnki.zgyz.1003-7969.240487 |
| 中文关键词: 棕榈油酸 脂多糖 急性肺损伤 炎症因子 JAK2/STAT3信号通路 |
| 英文关键词:palmitoleic acid lipopolysaccharide acute lung injury inflammatory factor JAK2/STAT3 signaling pathway |
| 基金项目:云南省重大科技专项计划（202202AE090006）；贵州省基础研究（自然科学）计划项目一般项目〔黔科合基础-ZK（2023）一般108〕；贵州大学实验室开放项目（SYSKF2025-037）;兴滇英才支持计划 |
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| 中文摘要: |
| 旨在为棕榈油酸（POA）在临床中的应用提供理论参考，探究POA对脂多糖（LPS）诱导的小鼠急性肺损伤的保护作用。将SPF雄性小鼠随机均分为5组〔对照组、LPS模型组、POA低剂量组、POA高剂量组、酪氨酸激酶抑制剂（AG490）组〕，POA低、高剂量组小鼠连续灌胃POA 4周，灌胃剂量分别为100、200 mg/kg，每日1次，AG490组在第4周灌胃AG490 1周，灌胃剂量10 mg/kg，每日1次，对照组和LPS模型组灌胃磷酸盐缓冲液，灌胃剂量为1 mL/只，每日1次，在第29天除对照组外所有小鼠采用腹腔注射5 mg/kg LPS诱导急性肺损伤，12 h后处死小鼠，取各组小鼠肺脏组织进行病理学，活性氧（ROS）水平、超氧化物歧化酶(SOD)活性、丙二醛（MDA）含量，肿瘤坏死因子-α（TNF-α）、白细胞介素-1β（IL-1β）和白细胞介素-6（IL-6）含量，磷酸化Janus激酶2（p-JAK2）、磷酸化信号转导和转录激活子3（p-STAT3） 蛋白表达和炎症因子mRNA转录水平检测。结果表明：与LPS模型组相比，POA低、高剂量组及AG490组小鼠肺脏组织病理损伤明显减轻，ROS水平显著降低（p<0.01），SOD活性显著升高（p<0.01），MDA含量显著下降（p<0.01）；TNF-α、IL-1β、IL-6含量显著减少（p<0.05或p<0.01）；p-JAK2、 p-STAT3蛋白表达和炎症因子mRNA转录水平显著下降（p<0.05或p<0.01）。综上，POA可减轻小鼠肺脏组织氧化应激水平和降低炎症因子含量，减轻LPS诱导的小鼠急性肺损伤程度，其机制可能与抑制Janus激酶2（JAK2）/信号转导和转录激活子3（JAK2/STAT3）信号通路有关。 |
| 英文摘要: |
| To provide theoretical references for the clinical application of palmitoleic acid (POA)， the protective effects of POA on lipopolysaccharide (LPS)-induced acute lung injury in mice was investigated. SPF male mice were randomly divided into five groups (control group, LPS model group, POA low-dose group, POA high-dose group, and AG490 group). Mice in the POA low-dose and high-dose groups were gavaged with POA for four consecutive weeks at doses of 100 mg/kg and 200 mg/kg respectively, once daily. Mice in the AG490 group were gavaged with AG490 for one week in the fourth week at a dose of 10 mg/kg, once daily. The control and LPS model groups were gavaged with phosphate-buffered saline at a dose of 1 mL per mouse, once daily. On the 29th day, all mice were intraperitoneally injected with 5 mg/kg LPS to induce acute lung injury except for the control group. After 12 h, the mice were sacrificed, and the lung tissues of mice in each group were collected for pathological examination, detection of reactive oxygen species (ROS) levels, superoxide dismutase (SOD) activity, malondialdehyde (MDA) content, tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) contents, as well as the protein expression of phosphorylated Janus kinase 2 (p-JAK2) and phosphorylated signal transducer and activator of transcription 3 (p-STAT3), and the transcriptional levels of inflammatory factor mRNA. The results showed that compared with the LPS model group, the lung tissue pathological damage in the POA low-and high-dose groups and the AG490 group was significantly reduced, ROS expression significantly decreased (p<0.01), SOD activity significantly increased (p<0.01), and MDA content significantly reduced (p<0.01); TNF-α, IL-1β, and IL-6 contents significantly decreased (p<0.05 or p<001); the protein expression of p- JAK2 and p-STAT3 and the transcriptional levels of inflammatory factor mRNA significantly decreased (p<0.05 or p<0.01). In conclusion, POA can reduce the oxidative stress level in mouse lung tissue and decrease the content of inflammatory factors, thereby alleviating the degree of LPS-induced acute lung injury in mice. The mechanism may be related to the inhibition of the JAK2/signal transducer and activator of transcription 3 (JAK2/STAT3) signaling pathway. |
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