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芒柄花素对脂多糖诱导的肺泡上皮细胞凋亡及炎症反应的抑制作用
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| 篇名： | 芒柄花素对脂多糖诱导的肺泡上皮细胞凋亡及炎症反应的抑制作用 |
| TITLE： | Inhibitory effects of formononetin on lipopolysaccharide-induced apoptosis and inflammatory response in alveolar epithelial cells |
| 摘要： | 目的 基于磷脂酰肌醇3激酶/蛋白激酶B（PI3K/Akt）信号通路，探讨芒柄花素对脂多糖（LPS）诱导的肺泡上皮细胞凋亡及炎症反应的抑制作用。方法体外培养肺癌人肺泡基底上皮细胞A549，分为对照组（不干预）、模型组（1μg/mLLPS）、芒柄花素不同浓度组（1μg/mLLPS+6.25、12.5、25、50μmol/L芒柄花素），检测各组细胞培养液中炎症因子（白细胞介素8、肿瘤坏死因子α）水平和细胞活力。另取A549细胞分为对照组、模型组（1μg/mLLPS）、LPS+25组（1μg/mLLPS+25μmol/L芒柄花素）、抑制剂组（1μg/mLLPS+20μmol/LLY294002）、芒柄花素+抑制剂组（1μg/mLLPS+25μmol/L芒柄花素+20μmol/LLY294002）和芒柄花素+激活剂组（1μg/mLLPS+25μmol/L芒柄花素+10μmol/LSC79），检测各组细胞炎症因子分泌水平和mRNA表达水平、细胞凋亡情况和PI3K/Akt信号通路关键蛋白表达情况。结果与模型组比较，25μmol/L的芒柄花素能显著降低细胞培养液中炎症因子水平，显著升高细胞活力（P＜0.05）。与对照组比较，模型组细胞中炎症因子的分泌水平和mRNA表达水平，细胞凋亡率，磷酸化Akt、磷酸化PI3K蛋白的相对表达量均显著升高（P＜0.05）；与模型组比较，LPS+25组和抑制剂组细胞上述指标均显著降低（P＜0.05）；与LPS+25组比较，芒柄花素+抑制剂组细胞上述指标均进一步降低，而芒柄花素+激活剂组细胞上述指标则显著升高（P＜0.05）。结论芒柄花素能够抑制LPS诱导的肺泡上皮细胞凋亡并改善其炎症反应，上述作用与抑制PI3K/Akt信号通路有关。 |
| ABSTRACT： | OBJECTIVE To investigate the inhibitory effects of formononetin on lipopolysaccharide （LPS）-induced apoptosis and inflammatory response in alveolar epithelial cells through phosphoinositide 3-kinase （PI3K）/protein kinase B （Akt） signaling pathway. METHODS Human lung cancer alveolar basal epithelial cells A549 were cultured in vitro and divided into control group （no intervention）， model group （1 μg/mL LPS）， different concentrations of formononetin groups （1 μg/mL LPS+6.25， 12.5， 25， 50 μmol/L formononetin）. The levels of inflammatory factors （interleukin-8， tumor necrosis factor-α） and cell viability were detected in each group. Another A549 cells were divided into control group， model group （1 μg/mL LPS）， LPS+25 group （1 μg/mL LPS+25 μmol/L formononetin）， inhibitor group （1 μg/mL LPS+20 μmol/L LY294002）， formononetin+inhibitor group （1 μg/mL LPS+25 μmol/L formononetin+20 μmol/L LY294002） and formononetin+activator group （1 μg/mL LPS+25 μmol/L formononetin+ 10 μmol/L SC79）. The secretion levels and mRNA expressions of inflammatory factors， cell apoptosis， and expressions of the key proteins of PI3K/Akt signaling pathway were detected in each group. RESULTS Compared with model group， the levels of inflammatory factors were decreased significantly after the intervention of 25 μmol/L of formononetin， and the cell viability was increased significantly （P＜0.05）. Compared with the control group， the secretion levels and mRNA expressions of inflammatory factors， apoptotic rate， and relative expressions of phosphorylated Akt and phosphorylated PI3K of the model group were increased significantly （P＜0.05）. Compared with the model group， the above indexes of the LPS+25 group and the inhibitor group were decreased significantly （P＜0.05）. Compared with the LPS+25 group， the above indicators of formononetin+inhibitor group were further decreased， while those of formononetin+activator group were increased significantly （P＜0.05）. CONCLUSIONS Formononetin can inhibit LPS-induced epithelial cell apoptosis and improve inflammatory response， and the mechanism may be related to the inhibition of the PI3K/Akt signaling pathway. |
| 期刊： | 2023年第34卷第22期 |
| 作者： | 林海；易金容；饶运帷 |
| AUTHORS： | LIN Hai，YI Jinrong，RAO Yunwei |
| 关键字： | 芒柄花素；肺泡上皮细胞；脂多糖；磷脂酰肌醇3激酶/蛋白激酶B信号通路；凋亡；炎症反应 |
| KEYWORDS： | formononetin； alveolar epithelial cells； lipopolysaccharide； phosphoinositide 3-kinase/protein kinase B signaling |
| 阅读数： | 42 次 |
| 本月下载数： | 6 次 |
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