Paudel U, Lee Y H, Kwon T H, Park N H, Yun B S, Hwang P H, Yi H K
Department of Oral Biochemistry, Institute of Oral Bioscience, BK21 program, School of Dentistry, Chonbuk National University, Jeonju, Korea.
Oral Dis. 2014 Nov;20(8):827-32. doi: 10.1111/odi.12266. Epub 2014 Aug 7.
The aim of this study was to elucidate the role of 6-6 bieckol (EB1) and pholorofucofuroeckol-A (EB5) from brown seaweed marine algae (Eisenia bicyclis) on lipopolysaccharide (LPS)-induced inflammation in human dental pulp cells (HDPCs).
The cytotoxicity of EB1 and EB5 was examined by MTT assay on LPS-induced human dental pulp cells. Their role on expression of inflammatory, odontogenic, and osteogenic molecules was determined by Western blot analysis. The dentin mineralization was checked by alkaline phosphatase activity.
The five compounds from E. bicyclis have different structure with non-cytotoxic in HDPCs. EB1 and EB5 showed anti-inflammatory properties and inhibited phosphorylated-extracellular signal-regulated kinase (p-ERK1/2) and phosphorylated-c-jun N-terminal kinases (p-JNK) without any cytotoxicity. In particular, EB1 inhibited cyclooxygenase-2 (COX-2) and p-ERK1/2 signaling, and EB5 inhibited only p-ERK1/2 signaling but not COX-2. Both compounds inhibited nuclear factor kappa-B (NF-κB) translocation. Furthermore, EB1 and EB5 increased dentinogenic and osteogenic molecules, and dentin mineralized via alkaline phosphatase activity (ALP) in LPS-induced HDPCs.
This study elucidates that EB1 and EB5 have different types of anti-inflammatory property and help in dentin formation. Therefore, these compounds derived from marine algae of E. bicyclis may be used as selective therapeutic strategies for pulpitis and oral diseases.
本研究旨在阐明从褐藻（昆布）中提取的6-6 二羟基-4,5-二苯并呋喃二聚体（EB1）和岩藻黄质-2,3 -环氧醚-A（EB5）对脂多糖（LPS）诱导的人牙髓细胞（HDPCs）炎症的作用。
通过MTT法检测EB1和EB5对LPS诱导的人牙髓细胞的细胞毒性。通过蛋白质免疫印迹分析确定它们对炎症、牙源性和成骨分子表达的作用。通过碱性磷酸酶活性检测牙本质矿化情况。
昆布中的五种化合物结构不同，对HDPCs无细胞毒性。EB1和EB5具有抗炎特性，可抑制磷酸化细胞外信号调节激酶（p-ERK1/2）和磷酸化c-jun氨基末端激酶（p-JNK），且无任何细胞毒性。特别是，EB1抑制环氧合酶-2（COX-2）和p-ERK1/2信号通路，而EB5仅抑制p-ERK1/2信号通路，不抑制COX-2。两种化合物均抑制核因子κB（NF-κB）易位。此外，EB1和EB5增加了牙本质生成和成骨分子，并且在LPS诱导的HDPCs中通过碱性磷酸酶活性（ALP）促进牙本质矿化。
本研究阐明了EB1和EB5具有不同类型的抗炎特性，并有助于牙本质形成。因此，这些从昆布海藻中提取的化合物可能用作牙髓炎和口腔疾病的选择性治疗策略。
