Department of Innovative Technologies in Medicine & Dentistry, University "G. d'Annunzio", Via dei Vestini, 66100, Chieti, Italy.
Department of Medicine & Aging Sciences, University "G. d'Annunzio", Via dei Vestini, 66100, Chieti, Italy.
Future Med Chem. 2024;16(14):1395-1411. doi: 10.1080/17568919.2024.2351293. Epub 2024 May 29.
In gastrointestinal (GI) diseases, lipopolysaccharide (LPS) exacerbates gut-barrier dysfunction and inflammation. Cinnamoyl derivatives show potential in mitigating LPS-induced inflammation. We assessed intestinal epithelial barrier function using -epithelial electrical resistance values and measured inflammatory mediators through real-time PCR and ELISA in Caco-2 cells. LPS treatment increased IL-6, IL-1β, TNF-α, PGE2 and TRL4 expression in Caco-2 cells. Pre-treatment with DM1 (1 or 10 μM) effectively countered LPS-induced TLR4 overexpression and reduced IL-6, IL-1β, TNF-α and PGE2 levels. DM1 holds promise in regulating inflammation and maintaining intestinal integrity by suppressing TLR4 and inflammatory mediators in Caco-2 cells. These findings suggest a potential therapeutic avenue for GI diseases.
在胃肠道（GI）疾病中，脂多糖（LPS）会加剧肠道屏障功能障碍和炎症。肉桂酰衍生物在减轻 LPS 诱导的炎症方面具有潜力。我们使用 -上皮电阻值评估肠道上皮屏障功能，并通过实时 PCR 和 ELISA 在 Caco-2 细胞中测量炎症介质。LPS 处理增加了 Caco-2 细胞中 IL-6、IL-1β、TNF-α、PGE2 和 TRL4 的表达。用 DM1（1 或 10 μM）预处理可有效拮抗 LPS 诱导的 TLR4 过表达，并降低 IL-6、IL-1β、TNF-α 和 PGE2 水平。DM1 通过抑制 TLR4 和 Caco-2 细胞中的炎症介质，具有调节炎症和维持肠道完整性的潜力。这些发现为 GI 疾病提供了一种潜在的治疗途径。
