[국내논문]Inhibitory Effects of Curcuma xanthorrhiza Supercritical Extract and Xanthorrhizol on LPS-Induced Inflammation in HGF-1 Cells and RANKL-Induced Osteoclastogenesis in RAW264.7 Cells원문보기
Periodontal disease is triggered by the host immune response to pathogens in the microbial biofilm. Worsening of periodontal disease destroys the tooth-supporting tissues and alveolar bone. As oral inflammation can induce systemic diseases in humans, it is important to prevent periodontal disease. I...
Periodontal disease is triggered by the host immune response to pathogens in the microbial biofilm. Worsening of periodontal disease destroys the tooth-supporting tissues and alveolar bone. As oral inflammation can induce systemic diseases in humans, it is important to prevent periodontal disease. In this study, we demonstrated that Curcuma xanthorrhiza supercritical extract (CXS) and its active compound, xanthorrhizol (XAN), exhibit anti-inflammatory effects on lipopolysaccharide (LPS)-treated human gingival fibroblast-1 cells and anti-osteoclastic effects on receptor activator of nuclear factor kappa B ligand (RANKL)-treated RAW264.7 cells. LPS-upregulated inflammatory factors, such as nuclear factor kappa B p65 and $interleukin-1{\beta}$, were prominently reduced by CXS and XAN. In addition, RANKL-induced osteoclastic factors, such as nuclear factor of activated T-cells c1, tartrate-resistant acid phosphatase, and cathepsin K, were decreased in the presence of CXS and XAN. CXS and XAN inhibited the mitogen-activated protein kinase (MAPK)/activator protein-1 (AP-1) signaling pathway. Collectively, these results provide evidence that CXS and XAN suppress LPS-induced inflammation and RANKL-induced osteoclastogenesis by suppressing the MAPK/AP-1 pathway.
Periodontal disease is triggered by the host immune response to pathogens in the microbial biofilm. Worsening of periodontal disease destroys the tooth-supporting tissues and alveolar bone. As oral inflammation can induce systemic diseases in humans, it is important to prevent periodontal disease. In this study, we demonstrated that Curcuma xanthorrhiza supercritical extract (CXS) and its active compound, xanthorrhizol (XAN), exhibit anti-inflammatory effects on lipopolysaccharide (LPS)-treated human gingival fibroblast-1 cells and anti-osteoclastic effects on receptor activator of nuclear factor kappa B ligand (RANKL)-treated RAW264.7 cells. LPS-upregulated inflammatory factors, such as nuclear factor kappa B p65 and $interleukin-1{\beta}$, were prominently reduced by CXS and XAN. In addition, RANKL-induced osteoclastic factors, such as nuclear factor of activated T-cells c1, tartrate-resistant acid phosphatase, and cathepsin K, were decreased in the presence of CXS and XAN. CXS and XAN inhibited the mitogen-activated protein kinase (MAPK)/activator protein-1 (AP-1) signaling pathway. Collectively, these results provide evidence that CXS and XAN suppress LPS-induced inflammation and RANKL-induced osteoclastogenesis by suppressing the MAPK/AP-1 pathway.
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가설 설정
In addition, many previous studies have shown that XAN reduced the phosphorylation of MAPK in CT26-bearing mice [13], 7,12-dimethylbenz[a]anthracene-treated mouse skin [14], and the liver of cisplatin-treated mice [15]. Based on previous studies, we hypothesized that C. xanthorrhiza and XAN have anti-periodontitis effects. To confirm our hypothesis, we evaluated whether C.
제안 방법
The cDNA was amplified with specific primers (Bioneer, Korea) (Table 1) using the GeneAmp PCR system 2700 (Applied Biosystems, USA) with the following procedure: denaturation for 30 sec at 94°C, annealing for 1 min, extension for 1 min at 72°C, and final extension for 5 min at 72°C.
To evaluate whether CXS and XAN inhibited osteoclast formation, we stained RANKL-stimulated RAW264.7 cells with TRAP solution and measured the activity of TRAP. The RANKL-treated group showed the formation of large and multinucleated osteoclasts, whereas the 10 μg/ml CXS- and 10 μM XAN-treated groups showed morphology similar to that of the normal group (Figs.
데이터처리
Differences between groups were assessed using a one-way analysis of variance, followed by the Scheffe’s test.
이론/모형
TRAP staining was performed using the Leukocyte Acid Phosphatase Kit (Sigma-Aldrich, USA) according to the manufacturer’s protocol.
To evaluate the cell viability of CXS and XAN, the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) colorimetric assay (Sigma-Aldrich, USA) was used. HGF-1 cells and RAW264.
Cell viability was measured by MTT assay. HGF-1 cells were co-treated with 1 μg/ml LPS and (A) CXS (1-20 μg/ml) or (B) XAN (1-20 μM) for 24 h.
성능/효과
Specifically, the transcripts of TRAP and c-Fos were decreased by 73.68% and 82.98%, respectively, in the 10 μg/ml CXS-treated group compared with that in the RANKL-treated group (Fig. 5A).
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