Periodontitis is caused by pathogens in the oral cavity. It is a chronic infectious disease that causes symptoms including gingival bleeding and tooth loss resulting from the destruction of periodontal tissues coupled with inflammation. Dendropanax morbiferus H.Lév (DM) is a natural product that exhibits various biological activities with few side effects. In this study, the potential of DM leaf hot-water extracts (DMWE) as a treatment for periodontitis was determined and its anti-oxidant and anti-inflammatory effects were evaluated. Compounds in DMWE were identified by high-performance liquid chromatography (HPLC) and nitric oxide (NO) and prostaglandin E₂ (PGE₂) production was measured in RAW 264.7 cells. We measured the gingival index and gingival sulcus depth, and micro-CT was performed in vivo using a ligature-induced periodontitis rat model, which is similar to human periodontitis. The DMWE-treated group exhibited a decrease in cytokine concentration and relieved the gingival index and gingival sulcus depth compared with the periodontitis-induced control group. In addition, micro-CT and histological analysis revealed that DMWE exhibited anti-inflammatory effects and improved alveolar bone loss in periodontitis-induced rats. These findings suggest that DMWE has excellent anti-oxidant and anti-inflammatory effects that protect and prevent periodontal tissue damage and tooth loss caused by the inflammatory response.

(1) Background: Rheumatoid arthritis (RA) is a chronic inflammatory condition known for its symptoms of joint damage and cartilage breakdown. Current treatments frequently result in adverse effects and show restricted efficacy in the long term. Dendropanax morbiferus, a plant recognized for its bioactive properties, demonstrates promise in the treatment of inflammatory conditions. The objective of this study was to examine the therapeutic properties of Dendropanax morbiferus Lév. water extract (DMWE) in RA through the utilization of in vitro and in vivo models. (2) Methods: Ultra-high-performance liquid chromatography (UPLC) analysis was used to identify bioactive compounds in DMWE. Antioxidant activity was evaluated using 1,1-diphenyl-2-picrylhydrazyl (DPPH) and 2,2-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid) diammonium salt (ABTS) radical-scavenging assays. The in vitro experiments involved the treatment of CHON-001 cells with DMWE in order to assess its impacts on inflammation and matrix metalloproteinase (MMP) expression. The impact of DMWE on the Janus Kinase 2 (JAK2) and Signal Transducer and Activator of Transcription (STAT) signaling pathways was also assessed. RA was induced in Balb/c mice who were subsequently treated with varying doses of DMWE to assess its impact on joint morphology, edema, and body weight. (3) Results: DMWE demonstrated substantial antioxidant activity and hindered the expression of MMP-2 and MMP-8 in chondrocytes treated with IL-1β. It additionally inhibited the JAK2/STAT pathway and diminished inflammatory responses. Treatment with DMWE in living organisms led to a decrease in joint swelling, improved weight regains, and maintained joint structure, with higher doses exhibiting effects similar to those of the positive control, dexamethasone (Dexa). (4) Conclusions: DMWE was found to have excellent in vitro antioxidant and anti-inflammatory activities. In an RA-induced mouse model, DMWE-3 (500 mg/kg BW) was found to effectively treat RA by reducing the concentration of pro-inflammatory factors and preventing joint deformation.