{"title":"希匹福林通过Akt磷酸化和NFκB通路对脂多糖诱导的急性肺损伤有保护作用","authors":"Yan-Yan Ng, Yung-Chuan Ho, Chi-Hua Yen, Shiuan-Shinn Lee, Ching-Chi Tseng, Sheng-Wen Wu, Yu-Hsiang Kuan","doi":"10.1002/tox.24383","DOIUrl":null,"url":null,"abstract":"<p><p>Acute lung injury (ALI) is a difficult condition to manage, especially when it is complicated by bacterial sepsis. Hibifolin, a flavonoid glycoside, has anti-inflammatory properties that make it a potential treatment for ALI. However, more research is needed to determine its effectiveness in LPS-induced ALI. In this study, male ICR mice were treated with hibifolin before LPS-induced ALI. Protein content and neutrophil count in bronchoalveolar lavage (BAL) fluid were measured by BCA assay and Giemsa staining method, respectively. The levels of proinflammatory cytokines and adhesive molecules were detected by ELISA assay. The expression of NFκB p65 phosphorylation, IκB degradation, and Akt phosphorylation was assessed by western blot assay. Hibifolin pre-treatment significantly reduced pulmonary vascular barrier dysfunction and neutrophil infiltration into the BAL fluid in LPS-induced ALI mice. In addition, LPS-induced expression of proinflammatory cytokines (IL-1β, IL-6, TNF-α) and adhesive molecules (ICAM-1, VCAM-1) within the BAL fluid were markedly reduced by hibifolin in LPS-induced ALI mice. More, hibifolin inhibited LPS-induced phosphorylation of NFκB p65, degradation of IκB, and phosphorylation of Akt in lungs with ALI mice. In conclusion, hibifolin shows promise in improving the pathophysiological features and proinflammatory responses of LPS-induced ALI in mice through the NFκB pathway and its upstream factor, Akt phosphorylation.</p>","PeriodicalId":11756,"journal":{"name":"Environmental Toxicology","volume":" ","pages":""},"PeriodicalIF":4.4000,"publicationDate":"2024-08-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Protective Effect of Hibifolin on Lipopolysaccharide-Induced Acute Lung Injury Through Akt Phosphorylation and NFκB Pathway.\",\"authors\":\"Yan-Yan Ng, Yung-Chuan Ho, Chi-Hua Yen, Shiuan-Shinn Lee, Ching-Chi Tseng, Sheng-Wen Wu, Yu-Hsiang Kuan\",\"doi\":\"10.1002/tox.24383\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Acute lung injury (ALI) is a difficult condition to manage, especially when it is complicated by bacterial sepsis. Hibifolin, a flavonoid glycoside, has anti-inflammatory properties that make it a potential treatment for ALI. However, more research is needed to determine its effectiveness in LPS-induced ALI. In this study, male ICR mice were treated with hibifolin before LPS-induced ALI. Protein content and neutrophil count in bronchoalveolar lavage (BAL) fluid were measured by BCA assay and Giemsa staining method, respectively. The levels of proinflammatory cytokines and adhesive molecules were detected by ELISA assay. The expression of NFκB p65 phosphorylation, IκB degradation, and Akt phosphorylation was assessed by western blot assay. Hibifolin pre-treatment significantly reduced pulmonary vascular barrier dysfunction and neutrophil infiltration into the BAL fluid in LPS-induced ALI mice. In addition, LPS-induced expression of proinflammatory cytokines (IL-1β, IL-6, TNF-α) and adhesive molecules (ICAM-1, VCAM-1) within the BAL fluid were markedly reduced by hibifolin in LPS-induced ALI mice. More, hibifolin inhibited LPS-induced phosphorylation of NFκB p65, degradation of IκB, and phosphorylation of Akt in lungs with ALI mice. In conclusion, hibifolin shows promise in improving the pathophysiological features and proinflammatory responses of LPS-induced ALI in mice through the NFκB pathway and its upstream factor, Akt phosphorylation.</p>\",\"PeriodicalId\":11756,\"journal\":{\"name\":\"Environmental Toxicology\",\"volume\":\" \",\"pages\":\"\"},\"PeriodicalIF\":4.4000,\"publicationDate\":\"2024-08-09\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Environmental Toxicology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1002/tox.24383\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"ENVIRONMENTAL SCIENCES\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Environmental Toxicology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1002/tox.24383","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"ENVIRONMENTAL SCIENCES","Score":null,"Total":0}
引用次数: 0
摘要
急性肺损伤(ALI)是一种难以控制的疾病,尤其是在并发细菌性败血症的情况下。Hibifolin是一种黄酮苷,具有抗炎特性,是治疗ALI的潜在药物。然而,要确定它对 LPS 诱导的 ALI 是否有效,还需要更多的研究。在这项研究中,雄性 ICR 小鼠在 LPS 诱导 ALI 前接受了希匹福林治疗。采用 BCA 法和 Giemsa 染色法分别测定了支气管肺泡灌洗液(BAL)中的蛋白质含量和中性粒细胞计数。酶联免疫吸附试验检测了促炎细胞因子和粘附分子的水平。免疫印迹法评估了 NFκB p65 磷酸化、IκB 降解和 Akt 磷酸化的表达。在LPS诱导的ALI小鼠中,Hibifolin预处理可明显减少肺血管屏障功能障碍和中性粒细胞向BAL液的浸润。此外,在 LPS 诱导的 ALI 小鼠中,希匹福林能明显降低 LPS 诱导的促炎细胞因子(IL-1β、IL-6、TNF-α)和粘附分子(ICAM-1、VCAM-1)在 BAL 液中的表达。此外,西比灵还能抑制 LPS 诱导的 ALI 小鼠肺内 NFκB p65 的磷酸化、IκB 的降解和 Akt 的磷酸化。总之,希匹福林有望通过NFκB通路及其上游因子Akt磷酸化改善LPS诱导的小鼠ALI的病理生理特征和促炎反应。
Protective Effect of Hibifolin on Lipopolysaccharide-Induced Acute Lung Injury Through Akt Phosphorylation and NFκB Pathway.
Acute lung injury (ALI) is a difficult condition to manage, especially when it is complicated by bacterial sepsis. Hibifolin, a flavonoid glycoside, has anti-inflammatory properties that make it a potential treatment for ALI. However, more research is needed to determine its effectiveness in LPS-induced ALI. In this study, male ICR mice were treated with hibifolin before LPS-induced ALI. Protein content and neutrophil count in bronchoalveolar lavage (BAL) fluid were measured by BCA assay and Giemsa staining method, respectively. The levels of proinflammatory cytokines and adhesive molecules were detected by ELISA assay. The expression of NFκB p65 phosphorylation, IκB degradation, and Akt phosphorylation was assessed by western blot assay. Hibifolin pre-treatment significantly reduced pulmonary vascular barrier dysfunction and neutrophil infiltration into the BAL fluid in LPS-induced ALI mice. In addition, LPS-induced expression of proinflammatory cytokines (IL-1β, IL-6, TNF-α) and adhesive molecules (ICAM-1, VCAM-1) within the BAL fluid were markedly reduced by hibifolin in LPS-induced ALI mice. More, hibifolin inhibited LPS-induced phosphorylation of NFκB p65, degradation of IκB, and phosphorylation of Akt in lungs with ALI mice. In conclusion, hibifolin shows promise in improving the pathophysiological features and proinflammatory responses of LPS-induced ALI in mice through the NFκB pathway and its upstream factor, Akt phosphorylation.
期刊介绍:
The journal publishes in the areas of toxicity and toxicology of environmental pollutants in air, dust, sediment, soil and water, and natural toxins in the environment.Of particular interest are:
Toxic or biologically disruptive impacts of anthropogenic chemicals such as pharmaceuticals, industrial organics, agricultural chemicals, and by-products such as chlorinated compounds from water disinfection and waste incineration;
Natural toxins and their impacts;
Biotransformation and metabolism of toxigenic compounds, food chains for toxin accumulation or biodegradation;
Assays of toxicity, endocrine disruption, mutagenicity, carcinogenicity, ecosystem impact and health hazard;
Environmental and public health risk assessment, environmental guidelines, environmental policy for toxicants.