首页|瓜蒌皮总皂苷调节PI3K/Akt/SIRT1信号通路减轻慢性阻塞性肺疾病大鼠的气道炎症

瓜蒌皮总皂苷调节PI3K/Akt/SIRT1信号通路减轻慢性阻塞性肺疾病大鼠的气道炎症

扫码查看
目的 探讨瓜蒌皮总皂苷通过调节PI3K/Akt/SIRT1 信号通路对慢性阻塞性肺疾病(COPD)大鼠气道炎症的影响.方法 SD 大鼠按照随机数字表法随机分成 5 组:对照组、模型组、瓜蒌皮总皂苷(300 mg/kg)组、LY294002(PI3K抑制剂,0.3 mg/kg)组、瓜蒌皮总皂苷(300 mg/kg)+LY294002(0.3 mg/kg)组,每组 12 只.除对照组外,其他组大鼠均构建COPD大鼠模型并给予药物干预.药物干预24h后,检测5 组大鼠肺功能;采用Giemsa染色进行肺泡灌洗液(BALF)中白细胞分类计数;HE染色观察 5 组大鼠肺组织病理形态变化,评测其损伤情况;试剂盒检测5 组大鼠BALF上清液和血清中IL-18、IL-17 水平;免疫印迹法检测各组大鼠肺组织中PI3K/Akt/SIRT1 信号通路蛋白表达.结果 与对照组大鼠的MV、PEF、Ri、白细胞数量、BALF上清液和血清中IL-18 和IL-17 水平、肺组织p-PI3K/PI3K、p-Akt/Akt及SIRT1 蛋白相对表达水平相比,模型组大鼠肺组织出现明显病理损伤,Ri、白细胞数量、BALF上清液和血清中IL-18 和IL-17 水平显著升高(P<0.05),MV、PEF、肺组织p-PI3K/PI3K,p-Akt/Akt及SIRT1 蛋白相对表达显著降低(P<0.05).与模型组和瓜蒌皮总皂苷+LY294002 组大鼠的MV、PEF、Ri、白细胞数量、BALF上清液和血清中IL-18 和IL-17 水平、肺组织p-PI3K/PI3K、p-Akt/Akt及SIRT1 蛋白相对表达水平相比,瓜蒌皮总皂苷组大鼠肺组织病理损伤症状均减轻,Ri、白细胞数量、BALF上清液和血清中IL-18 和IL-17 水平均降低(P<0.05),MV、PEF、肺组织p-PI3K/PI3K、p-Akt/Akt及SIRT1 蛋白相对表达均升高(P<0.05);LY294002 组大鼠肺组织病理损伤症状均加重,Ri、白细胞数量、BALF上清液和血清中IL-18 和IL-17 水平均升高(P<0.05),MV、PEF、肺组织p-PI3K/PI3K、p-Akt/Akt及SIRT1 蛋白蛋白相对表达均降低(P<0.05).结论 瓜蒌皮总皂苷可能通过激活PI3K/Akt/SIRT1 信号通路,减轻COPD大鼠气道炎症,改善肺组织损伤,修复肺功能.
Total saponins extracted from Pericarpium trichosanthis reduce airway inflammation in rats with chronic obstructive pulmonary disease by regulating the PI3K/Akt/SIRT1 signaling pathway
Objective To investigate the effect of total saponins extracted from Pericarpium trichosanthis on airway inflammation in rats with chronic obstructive pulmonary disease(COPD)by regulating the phosphatidylinositol 3-kinase(PI3K)/protein kinase B(Akt)/Sirtuin 1(SIRT1)signaling pathway.Methods Rats were randomly divided into control group(blank control),model group(COPD modeling),total saponins group(COPD modeling + 300mg/kg total saponins),LY294002 group(COPD modeling + 0.3mg/kg PI3K inhibitor LY294002),and total saponins + LY294002 group(COPD modeling + 300mg/kg total saponins + 0.3mg/kg LY294002),with 12 rats in each group.Except for the control group,rats in other groups were constructed as COPD models and given drug intervention.After 24 hours of drug intervention,lung function of rats in each group was detected.Giemsa staining was used for the classification and counting of white blood cells in alveolar lavage fluid(BALF).The hematoxylin and eosin(H&E)staining was performed to observe the pathological changes of the lung tissue.Commercial kits were used to detect the levels of interleukin 18(IL-18)and IL-17 in the BALF and serum of rats in each group.Western blotting was used to detect the expressions of proteins in the PI3K/Akt/SIRT1 signaling pathway in the lung tissues of rats in each group.Results Compared with those of control group,rats in the model group presented obvious pathological damages in lung tissues,significantly higher Ri,WBC and IL-18 and IL-17 levels in BALF and serum,and lower MV,PEF and protein expressions of p-PI3K/PI3K,p-Akt/Akt and SIRT1 in lung tissues(P<0.05).Compared with those of model group and total saponins + LY294002 group,rats in the total saponins group presented alleviated pathological damages in lung tissues,significantly lower Ri,WBC and IL-18 and IL-17 levels in BALF and serum(P<0.05),and higher MV,PEF and protein expressions of p-PI3K/PI3K,p-Akt/Akt and SIRT1 in lung tissues(P<0.05).Rats in the LY294002 group presented aggravated pathological damages in lung tissues,significantly higher Ri,WBC and IL-18 and IL-17 levels in BALF and serum,and lower MV,PEF and protein expressions of p-PI3K/PI3K,p-Akt/Akt and SIRT1 in lung tissues(P<0.05).Conclusion The total saponins extracted from Pericarpium trichosanthis can reduce airway inflammation,improve lung tissue damage and repair lung function in COPD rats by activating the PI3K/Akt/SIRT1 signaling pathway.

total saponins extracted from Pericarpium trichosanthisphosphatidylinositol 3-kinase(PI3K)/protein kinase B(Akt)/Sirtuin 1(SIRT1)chronic obstructive pulmonary diseaseairway inflammation

周利君、郭红荣、王红娟、徐建群、方思

展开 >

430074 湖北省武汉市第三医院呼吸与危重症医学科

430074 湖北省武汉市第三医院呼吸内科

瓜蒌皮总皂苷 PI3K/Akt/SIRT1 慢性阻塞性肺疾病 气道炎症

2024

河北医药
河北省医学情报研究所

河北医药

CSTPCD
影响因子:1.075
ISSN:1002-7386
年,卷(期):2024.46(6)
  • 20