Effects of Korean Propolis Extracts on Porphyromonas gingivalis Lipopolysaccharide-Induced Inflammatory Responses in RAW 264.7 Cells
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Background: Porphyromonas gingivalis is a primary etiological agent of chronic periodontitis in adults, and its lipopolysaccharide (LPS) elicits a strong inflammatory response that contributes to periodontal tissue destruction. Propolis has been reported to exhibit multiple pharmacological activities, including anti-inflammatory, antibacterial, and antioxidant effects. This study aimed to evaluate the effects of propolis extracts (PEs) collected from different regions of South Korea on LPS from P. gingivalis (LPS-PG)-induced inflammatory responses. Methods: Inflammatory responses were induced in RAW 264.7 macrophages using LPS-PG, followed by treatment with PEs from eight different regions of South Korea at varying concentrations. Cell viability was assessed using the Cell Counting Kit-8 assay, and the production of nitric oxide (NO) and prostaglandin E2 (PGE2), key inflammatory mediators, was quantified using the Griess reaction and enzyme-linked immunosorbent assay, respectively. Protein expression levels of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) were assessed by Western blot analysis. Results: All PEs dose-dependently inhibited LPS-PG-induced NO and PGE2 production within nontoxic concentration ranges in RAW 264.7 cells (p＜0.05). Furthermore, PEs at a concentration of 20 μg/ml markedly reduced the protein expression of iNOS and COX-2, which regulate the production of NO and PGE2. Conclusion: Korean propolis effectively suppresses LPS-PG–induced inflammatory responses, with comparable inhibitory effects observed across all regional extracts. These findings suggest that Korean propolis may serve as a natural anti-inflammatory agent for adjunctive prevention and treatment of periodontitis.
Abstract
Background: Porphyromonas gingivalis is a primary etiological agent of chronic periodontitis in adults, and its lipopolysaccharide (LPS) elicits a strong inflammatory response that contributes to periodontal tissue destruction. Propolis has been reported to exhibit multiple pharmacological activities, including anti-inflammatory, antibacterial, and antioxidant effects. This study aimed to evaluate the effects of propolis extracts (PEs) collected from different regions of South Korea on LPS from P. gingivalis (LPS-PG)-induced inflammatory responses. Methods: Inflammatory responses were induced in RAW 264.7 macrophages using LPS-PG, followed by treatment with PEs from eight different regions of South Korea at varying concentrations. Cell viability was assessed using the Cell Counting Kit-8 assay, and the production of nitric oxide (NO) and prostaglandin E2 (PGE2), key inflammatory mediators, was quantified using the Griess reaction and enzyme-linked immunosorbent assay, respectively. Protein expression levels of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) were assessed by Western blot analysis. Results: All PEs dose-dependently inhibited LPS-PG-induced NO and PGE2 production within nontoxic concentration ranges in RAW 264.7 cells (p＜0.05). Furthermore, PEs at a concentration of 20 μg/ml markedly reduced the protein expression of iNOS and COX-2, which regulate the production of NO and PGE2. Conclusion: Korean propolis effectively suppresses LPS-PG–induced inflammatory responses, with comparable inhibitory effects observed across all regional extracts. These findings suggest that Korean propolis may serve as a natural anti-inflammatory agent for adjunctive prevention and treatment of periodontitis.