| Autor: |
Kim HJ; Laboratory Animal Resource Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon 34141, Republic of Korea., Choi JH; Laboratory Animal Resource Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon 34141, Republic of Korea., Hwang JH; Laboratory Animal Resource Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon 34141, Republic of Korea., Kim KS; Laboratory Animal Resource Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon 34141, Republic of Korea., Noh JR; Laboratory Animal Resource Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon 34141, Republic of Korea., Choi DH; Laboratory Animal Resource Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon 34141, Republic of Korea., Moon SJ; Laboratory Animal Resource Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon 34141, Republic of Korea., Kim HY; Laboratory Animal Resource Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon 34141, Republic of Korea., Kim SW; Laboratory Animal Center, Osong Medical Innovation Foundation, Cheongju, Chungcheongbuk‑do 28160, Republic of Korea., Choi S; International Biological Material Research Center, Natural Medicine Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon 34141, Republic of Korea., Eum SM; International Biological Material Research Center, Natural Medicine Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon 34141, Republic of Korea., Bach TT; Institute of Ecology and Biological Resources, Vietnam Academy of Science and Technology, Hanoi, Vietnam., Rho J; Department of Microbiology and Molecular Biology, Chungnam National University, Daejeon 34134, Republic of Korea., Lee JY; Korea Bioactive Natural Material Bank, Research Institute of Pharmaceutical Sciences, College of Pharmacy, Seoul National University, Seoul 08826, Republic of Korea., Park JG; Korea Bioactive Natural Material Bank, Research Institute of Pharmaceutical Sciences, College of Pharmacy, Seoul National University, Seoul 08826, Republic of Korea., Oh SR; University of Science and Technology, Daejeon 34113, Republic of Korea., Lee CH; Laboratory Animal Resource Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon 34141, Republic of Korea., Oh WK; Korea Bioactive Natural Material Bank, Research Institute of Pharmaceutical Sciences, College of Pharmacy, Seoul National University, Seoul 08826, Republic of Korea., Kim YH; Laboratory Animal Resource Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon 34141, Republic of Korea. |
| Abstrakt: |
Melicope ptelefolia has been traditionally used to treat rheumatism and fever. The present study aimed to investigate the therapeutic effect of 3,5‑di‑C‑β‑D‑glucopyranosyl phloroacetophenone (βGP), a main component of M. ptelefolia, on rheumatoid arthritis (RA). A model of collagen‑induced arthritis (CIA) was established in mice using the RAW 264.7 murine macrophage cell line and mouse embryonic fibroblasts (MEFs). The clinical scores of arthritis, swelling, histopathological findings, and micro‑computed tomography in CIA mouse paws were assessed. The levels of anti‑type II collagen antibody and cytokines were determined in the plasma and cell culture supernatant, respectively. Protein and gene expression levels were analyzed by western blot and reverse transcription‑quantitative polymerase chain reaction analyses. βGP significantly decreased the gross arthritic scores of CIA mice and joint swelling, and decreased articular inflammation, cartilage degradation and bone erosion. However, βGP did not exert any effect on anti‑type II collagen immunoglobulin G plasma levels or inflammatory cytokine expression in macrophages. βGP significantly suppressed the expression of interleukin‑6 and leukemia inhibitory factor and decreased the phosphorylation of signal transducer and activator of transcription 3, and expression of receptor activator of nuclear factor‑κB ligand in tumor necrosis factor‑α‑stimulated MEFs and in CIA mouse paws. Osteoclast‑related gene expression was significantly reduced in CIA mouse paws. Taken together, βGP suppressed the development of RA by regulating the activation of synovial fibroblasts. |
