{"title":"炔诺酮可减轻 LPS 诱导的 RAW264.7 细胞和卵清蛋白诱导的哮喘小鼠体内的炎症细胞因子。","authors":"Junyan Chen, Xiaohong Liu","doi":"10.1002/jbt.23836","DOIUrl":null,"url":null,"abstract":"<p>This study examines the anti-inflammatory activity of cynaropicrin against lipopolysaccharide (LPS) in vitro and ovalbumin (OVA)-challenged asthma in mice. Cynaropicrin's antimicrobial effects were tested on <i>Escherichia coli (E. coli)</i> and <i>Streptococcus pyogenes (S. pyogenes)</i> using the disc diffusion technique. Cytotoxicity was assessed with an (3-(4, 5-dimethylthiazolyl-2)-2, 5-diphenyltetrazolium bromide) assay. The anti-inflammatory property was evaluated in LPS-induced RAW264.7 cells, while OVA-challenged asthmatic mice were treated with 10 mg/kg of cynaropicrin. Key inflammatory and antioxidant markers were quantified, and lung histology was examined to confirm therapeutic roles. The antimicrobial studies proved that cynaropicrin effectively inhibited the growth of <i>E. coli</i> and <i>S. pyogenes</i>. Cynaropicrin displayed no cytotoxicity on RAW264.7 cells. Furthermore, it significantly inhibited inflammatory cytokine synthesis upon LPS induction. Cynaropicrin treatment decreased the inflammatory cell counts and also suppressed specific allergic markers in OVA-challenged mice. It also decreased nitric oxide and myeloperoxidase levels and reduced pulmonary edema. Cynaropicrin increased antioxidant levels and decreased proinflammatory cytokines in the asthmatic mice. Lung histological examination confirms the ameliorative potency of cynaropicrin against OVA-induced asthmatic pulmonary inflammation in mice. Our findings suggest cynaropicrin possesses significant ameliorative potency against allergen-induced pulmonary inflammation.</p>","PeriodicalId":3,"journal":{"name":"ACS Applied Electronic Materials","volume":null,"pages":null},"PeriodicalIF":4.3000,"publicationDate":"2024-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Cynaropicrin attenuates inflammatory cytokines in LPS-induced RAW264.7 cells and ovalbumin-induced asthmatic mice\",\"authors\":\"Junyan Chen, Xiaohong Liu\",\"doi\":\"10.1002/jbt.23836\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p>This study examines the anti-inflammatory activity of cynaropicrin against lipopolysaccharide (LPS) in vitro and ovalbumin (OVA)-challenged asthma in mice. Cynaropicrin's antimicrobial effects were tested on <i>Escherichia coli (E. coli)</i> and <i>Streptococcus pyogenes (S. pyogenes)</i> using the disc diffusion technique. Cytotoxicity was assessed with an (3-(4, 5-dimethylthiazolyl-2)-2, 5-diphenyltetrazolium bromide) assay. The anti-inflammatory property was evaluated in LPS-induced RAW264.7 cells, while OVA-challenged asthmatic mice were treated with 10 mg/kg of cynaropicrin. Key inflammatory and antioxidant markers were quantified, and lung histology was examined to confirm therapeutic roles. The antimicrobial studies proved that cynaropicrin effectively inhibited the growth of <i>E. coli</i> and <i>S. pyogenes</i>. Cynaropicrin displayed no cytotoxicity on RAW264.7 cells. Furthermore, it significantly inhibited inflammatory cytokine synthesis upon LPS induction. Cynaropicrin treatment decreased the inflammatory cell counts and also suppressed specific allergic markers in OVA-challenged mice. It also decreased nitric oxide and myeloperoxidase levels and reduced pulmonary edema. Cynaropicrin increased antioxidant levels and decreased proinflammatory cytokines in the asthmatic mice. Lung histological examination confirms the ameliorative potency of cynaropicrin against OVA-induced asthmatic pulmonary inflammation in mice. Our findings suggest cynaropicrin possesses significant ameliorative potency against allergen-induced pulmonary inflammation.</p>\",\"PeriodicalId\":3,\"journal\":{\"name\":\"ACS Applied Electronic Materials\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":4.3000,\"publicationDate\":\"2024-09-22\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"ACS Applied Electronic Materials\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://onlinelibrary.wiley.com/doi/10.1002/jbt.23836\",\"RegionNum\":3,\"RegionCategory\":\"材料科学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"ENGINEERING, ELECTRICAL & ELECTRONIC\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"ACS Applied Electronic Materials","FirstCategoryId":"3","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1002/jbt.23836","RegionNum":3,"RegionCategory":"材料科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"ENGINEERING, ELECTRICAL & ELECTRONIC","Score":null,"Total":0}
引用次数: 0
摘要
本研究探讨了犬尿苷对体外脂多糖(LPS)和卵清蛋白(OVA)诱导的小鼠哮喘的抗炎活性。使用圆盘扩散技术测试了犬尿苷对大肠杆菌(E. coli)和化脓性链球菌(S. pyogenes)的抗菌效果。细胞毒性采用(3-(4,5-二甲基噻唑基-2)-2,5-二苯基溴化四氮唑)测定法进行评估。在 LPS 诱导的 RAW264.7 细胞中对抗炎性进行了评估,而 OVA 攻击性哮喘小鼠则接受了 10 毫克/千克的卡诺匹克林治疗。对主要的炎症和抗氧化标记物进行了量化,并对肺组织学进行了检查,以确认其治疗作用。抗菌研究证明,卡泊三醇能有效抑制大肠杆菌和化脓性链球菌的生长。卡马西平对 RAW264.7 细胞无细胞毒性。此外,它还能明显抑制 LPS 诱导的炎症细胞因子的合成。在 OVA 攻击小鼠体内,Cynaropicrin 处理可减少炎症细胞数量并抑制特定的过敏标记物。它还能降低一氧化氮和髓过氧化物酶水平,减轻肺水肿。炔诺酮可提高哮喘小鼠的抗氧化水平,减少促炎细胞因子。肺组织学检查证实了卡那霉素对 OVA 诱导的小鼠哮喘性肺部炎症的改善作用。我们的研究结果表明,卡泊三醇对过敏原诱发的肺部炎症具有显著的改善作用。
Cynaropicrin attenuates inflammatory cytokines in LPS-induced RAW264.7 cells and ovalbumin-induced asthmatic mice
This study examines the anti-inflammatory activity of cynaropicrin against lipopolysaccharide (LPS) in vitro and ovalbumin (OVA)-challenged asthma in mice. Cynaropicrin's antimicrobial effects were tested on Escherichia coli (E. coli) and Streptococcus pyogenes (S. pyogenes) using the disc diffusion technique. Cytotoxicity was assessed with an (3-(4, 5-dimethylthiazolyl-2)-2, 5-diphenyltetrazolium bromide) assay. The anti-inflammatory property was evaluated in LPS-induced RAW264.7 cells, while OVA-challenged asthmatic mice were treated with 10 mg/kg of cynaropicrin. Key inflammatory and antioxidant markers were quantified, and lung histology was examined to confirm therapeutic roles. The antimicrobial studies proved that cynaropicrin effectively inhibited the growth of E. coli and S. pyogenes. Cynaropicrin displayed no cytotoxicity on RAW264.7 cells. Furthermore, it significantly inhibited inflammatory cytokine synthesis upon LPS induction. Cynaropicrin treatment decreased the inflammatory cell counts and also suppressed specific allergic markers in OVA-challenged mice. It also decreased nitric oxide and myeloperoxidase levels and reduced pulmonary edema. Cynaropicrin increased antioxidant levels and decreased proinflammatory cytokines in the asthmatic mice. Lung histological examination confirms the ameliorative potency of cynaropicrin against OVA-induced asthmatic pulmonary inflammation in mice. Our findings suggest cynaropicrin possesses significant ameliorative potency against allergen-induced pulmonary inflammation.