扁柏酚通过激活细胞外信号调节激酶（ERK）和p38丝裂原活化蛋白激酶（p38MAPK）以及上调缺氧诱导因子-1α（HIF-1α）来增强牙髓细胞的血管生成潜力。
Hinokitiol increases the angiogenic potential of dental pulp cells through ERK and p38MAPK activation and hypoxia-inducible factor-1α (HIF-1α) upregulation.
作者信息
Kim Mi-Kyoung, Park Hyun-Joo, Kim Yong-Deok, Ryu Mi Heon, Takata Takashi, Bae Soo-Kyung, Bae Moon-Kyoung
机构信息
Department of Oral Physiology, School of Dentistry, Pusan National University, Yangsan 626-870, South Korea.
Department of Oral Physiology, School of Dentistry, Pusan National University, Yangsan 626-870, South Korea; Department of Dental Pharmacology, School of Dentistry, Pusan National University, Yangsan 626-870, South Korea.
出版信息
Arch Oral Biol. 2014 Feb;59(2):102-10. doi: 10.1016/j.archoralbio.2013.10.009. Epub 2013 Oct 31.
Hinokitiol, a natural iron-chelating agent, is known to have diverse biological and pharmacological activities in various cell types. However, the effect of hinokitiol on dental pulp cells has not yet been reported. In this study, hinokitiol increases hypoxia-inducible factor-1α (HIF-1α) protein levels and vascular endothelial growth factor (VEGF) secretion in human dental pulp cells. The extracellular-signal-regulated kinase (ERK) and p38 mitogen-activated protein kinase (MAPK) pathways are involved in hinokitiol-induced HIF-1α protein expression in dental pulp cells. Conditioned media from hinokitiol-treated pulp cells enhances angiogenesis in vitro and in vivo. Overall, these results show that hinokitiol promotes ERK and p38MAPK activation and HIF-1α-induced VEGF production, thus increasing the angiogenic potential of dental pulp cells.
扁柏酚是一种天然铁螯合剂，已知在各种细胞类型中具有多种生物学和药理活性。然而，扁柏酚对牙髓细胞的影响尚未见报道。在本研究中，扁柏酚可增加人牙髓细胞中缺氧诱导因子-1α（HIF-1α）蛋白水平和血管内皮生长因子（VEGF）分泌。细胞外信号调节激酶（ERK）和p38丝裂原活化蛋白激酶（MAPK）信号通路参与了扁柏酚诱导的牙髓细胞中HIF-1α蛋白表达。经扁柏酚处理的牙髓细胞的条件培养基可增强体内外血管生成。总体而言，这些结果表明，扁柏酚可促进ERK和p38MAPK激活以及HIF-1α诱导的VEGF产生，从而增加牙髓细胞的血管生成潜力。
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