Department of Regenerative Dental Medicine, Tokushima University Graduate School of Biomedical Sciences, 3-18-15 Kuramoto-cho, Tokushima, Tokushima, 770-8504, Japan.
Department of Oral Health Care Promotion, Tokushima University Graduate School of Biomedical Sciences, Tokushima, Tokushima, Japan.
Mol Biol Rep. 2024 Jan 28;51(1):222. doi: 10.1007/s11033-023-09204-8.
Cardamonin is classified as a natural chalcone, and has been reported to possess various bioactive effects. However, there have been limited attempts to utilize cardamonin in the treatment of periodontitis. This study aimed to investigate whether cardamonin has anti-inflammatory effects on human periodontal ligament cells (HPDLCs), which are a component cell of periodontal tissue. Specifically, the study seeks to determine whether cardamonin affects the expression of inflammatory mediators, such as cytokines and adhesion molecules, induced by interleukin-1β (IL-1β) in HPDLCs, as well as the signaling pathways activated by IL-1β.
Cytokine and chemokine levels in supernatants of HPDLCs were measured by ELISA. Western blot analysis was used to measure protein expression and signal transduction pathway activation in HPDLCs.
We found that IL-1β-induced CC chemokine ligand (CCL)2, CCL5, CCL20, CXC-chemokine ligand (CXCL)10, and interleukin (IL)-6 production and intercellular adhesion molecule (ICAM)-1 and cyclooxygenase (COX)-2 expression in HPDLCs were suppressed by cardamonin treatment. We also found that cardamonin suppressed IL-1β-activated nuclear factor (NF)-κB pathway, and the phosphorylation of signal transducer and activator of transcription (STAT)3. Furthermore, cardamonin treatment enhanced the expression of the antioxidant enzymes, heme oxygenase (HO)-1 and NAD(P)H dehydrogenase [quinone] 1 (NQO1), in HPDLCs.
In this study, we found that cardamonin could suppress the production of inflammatory mediators in HPDLCs as well as the activation of several signaling pathways induced by IL-1β treatment.
小豆蔻明被归类为天然查耳酮，已被报道具有多种生物活性作用。然而，利用小豆蔻明治疗牙周炎的尝试有限。本研究旨在探讨小豆蔻明对人牙周韧带细胞（HPDLC）是否具有抗炎作用，HPDLC 是牙周组织的组成细胞。具体而言，本研究旨在确定小豆蔻明是否会影响 HPDLC 中由白细胞介素 1β（IL-1β）诱导的炎症介质（如细胞因子和粘附分子）的表达，以及 IL-1β 激活的信号通路。
通过 ELISA 测量 HPDLC 上清液中的细胞因子和趋化因子水平。使用 Western blot 分析测量 HPDLC 中的蛋白质表达和信号转导通路激活。
我们发现，小豆蔻明处理可抑制 IL-1β诱导的 HPDLC 中 C 型趋化因子配体（CCL）2、CCL5、CCL20、CXC 趋化因子配体（CXCL）10 和白细胞介素（IL）-6 的产生以及细胞间粘附分子（ICAM）-1 和环氧化酶（COX）-2 的表达。我们还发现，小豆蔻明抑制了 IL-1β激活的核因子（NF）-κB 途径和信号转导和转录激活因子（STAT）3 的磷酸化。此外，小豆蔻明处理增强了 HPDLC 中抗氧化酶血红素加氧酶（HO）-1 和 NAD（P）H 脱氢酶[醌]1（NQO1）的表达。
在这项研究中，我们发现小豆蔻明可以抑制 HPDLC 中炎症介质的产生以及 IL-1β 处理诱导的几种信号通路的激活。
