PDF(Pubmed)
Abstract：
UNASSIGNED: Diabetes has been recognized as an independent risk factor for periodontitis. Increasing evidences indicate that hyperglycemia aggravates inflammatory response of human periodontal ligament cells (hPDLCs). Carbon monoxide-releasing molecule-3 (CORM-3) is a water-soluble compound that can release carbon monoxide (CO) in a controllable manner. CORM-3 has been shown the anti-inflammatory effect in different cell lineages.
UNASSIGNED: We stimulated periodontal ligament cells with LPS and high glucose. The expression of inflammatory cytokine was detected by ELISA. RT-qPCR, Western blot and immunofluorescence were used to detect the expression of TLR2, TLR4, RAGE and the activation of NF-κB pathway. We performed silencing and overexpression treatment of RAGE targeting the role of RAGE. We performed the immunostaining of paraffin sections of the periodontitis model in diabetes rats.
UNASSIGNED: The results showed that CORM-3 significantly inhibited the expression of inflammatory cytokine in hPDLCs stimulated with LPS and high glucose. CORM-3 also inhibited LPS and high glucose-induced expression of RAGE/NF-κB pathway and TLR2/TLR4/NF-κB pathway. Silence of RAGE resulted in significantly decreased expression of proteins above. Overexpression of RAGE significantly enhanced the expression of these factors. CORM-3 abrogated the effect of RAGE partially. In animal model, CORM-3 suppressed the inflammatory response of periodontal tissues in experimental periodontitis of diabetic rats.
UNASSIGNED: Our research proved CORM-3 reduced the inflammatory response via RAGE/NF-κB pathway and TLR2/TLR4/NF-κB pathway in the process of high glucose exacerbated periodontitis. These findings demonstrated the role of RAGE in the process of high glucose exacerbated periodontitis and suggested that CORM3 be a potential therapeutic strategy for the treatment of diabetes patients with periodontitis.
UNASSIGNED: We stimulated periodontal ligament cells with LPS and high glucose. The expression of inflammatory cytokine was detected by ELISA. RT-qPCR, Western blot and immunofluorescence were used to detect the expression of TLR2, TLR4, RAGE and the activation of NF-κB pathway. We performed silencing and overexpression treatment of RAGE targeting the role of RAGE. We performed the immunostaining of paraffin sections of the periodontitis model in diabetes rats.
UNASSIGNED: The results showed that CORM-3 significantly inhibited the expression of inflammatory cytokine in hPDLCs stimulated with LPS and high glucose. CORM-3 also inhibited LPS and high glucose-induced expression of RAGE/NF-κB pathway and TLR2/TLR4/NF-κB pathway. Silence of RAGE resulted in significantly decreased expression of proteins above. Overexpression of RAGE significantly enhanced the expression of these factors. CORM-3 abrogated the effect of RAGE partially. In animal model, CORM-3 suppressed the inflammatory response of periodontal tissues in experimental periodontitis of diabetic rats.
UNASSIGNED: Our research proved CORM-3 reduced the inflammatory response via RAGE/NF-κB pathway and TLR2/TLR4/NF-κB pathway in the process of high glucose exacerbated periodontitis. These findings demonstrated the role of RAGE in the process of high glucose exacerbated periodontitis and suggested that CORM3 be a potential therapeutic strategy for the treatment of diabetes patients with periodontitis.
摘要：
■糖尿病已被认为是牙周炎的独立危险因素。越来越多的证据表明，高血糖会加重人牙周膜细胞（hPDLCs）的炎症反应。一氧化碳释放分子3（CORM-3）是一种水溶性化合物，可以以可控方式释放一氧化碳（CO）。已显示CORM-3在不同细胞系中具有抗炎作用。
■我们用LPS和高糖刺激牙周膜细胞。ELISA法检测炎性细胞因子的表达。RT-qPCR,免疫印迹法和免疫荧光法检测TLR2、TLR4、RAGE的表达及NF-κB通路的激活。我们针对RAGE的作用进行了RAGE的沉默和过表达治疗。我们对糖尿病大鼠牙周炎模型的石蜡切片进行了免疫染色。
■结果显示CORM-3显著抑制LPS和高糖刺激的hPDLCs中炎性细胞因子的表达。CORM-3还抑制LPS和高糖诱导的RAGE/NF-κB通路和TLR2/TLR4/NF-κB通路的表达。RAGE的沉默导致上述蛋白质的表达显着降低。RAGE的过表达显著增强了这些因子的表达。CORM-3部分消除了RAGE的作用。在动物模型中,CORM-3抑制糖尿病大鼠实验性牙周炎中牙周组织的炎症反应。
■我们的研究证明CORM-3通过RAGE/NF-κB通路和TLR2/TLR4/NF-κB通路减轻高糖加重牙周炎过程中的炎症反应。这些发现证明了RAGE在高糖加重牙周炎过程中的作用，并表明CORM3是治疗糖尿病伴牙周炎患者的潜在治疗策略。
■我们用LPS和高糖刺激牙周膜细胞。ELISA法检测炎性细胞因子的表达。RT-qPCR,免疫印迹法和免疫荧光法检测TLR2、TLR4、RAGE的表达及NF-κB通路的激活。我们针对RAGE的作用进行了RAGE的沉默和过表达治疗。我们对糖尿病大鼠牙周炎模型的石蜡切片进行了免疫染色。
■结果显示CORM-3显著抑制LPS和高糖刺激的hPDLCs中炎性细胞因子的表达。CORM-3还抑制LPS和高糖诱导的RAGE/NF-κB通路和TLR2/TLR4/NF-κB通路的表达。RAGE的沉默导致上述蛋白质的表达显着降低。RAGE的过表达显著增强了这些因子的表达。CORM-3部分消除了RAGE的作用。在动物模型中,CORM-3抑制糖尿病大鼠实验性牙周炎中牙周组织的炎症反应。
■我们的研究证明CORM-3通过RAGE/NF-κB通路和TLR2/TLR4/NF-κB通路减轻高糖加重牙周炎过程中的炎症反应。这些发现证明了RAGE在高糖加重牙周炎过程中的作用，并表明CORM3是治疗糖尿病伴牙周炎患者的潜在治疗策略。
