Houttuynia cordata suppresses the Aggregatibacter actinomycetemcomitans-induced increase of inflammatory-related genes in cultured human gingival epithelial cells

Background/purpose: Periodontitis is an infectious inflammatory disease. Gingival epithelium is the primary barrier against invasion of microorganisms and produces inflammatory cytokines. Our previous studies showed that regulating the function on the gingival epithelium was useful in suppressing the onset of periodontal disease. Houttuynia cordata is commonly used in traditional oriental medicine formulations and has been associated with a broad range of pharmacological activities. To investigate the potential of H. cordata as a preventive medicine, we examined the effect of H. cordata on the expression of inflammatory-related genes in human gingival epithelial cells (HGECs) exposed to Aggregatibacter actinomycetemcomitans. Materials and methods: The messenger RNA (mRNA) levels of matrix metalloproteinase-3 (MMP-3), interleukin (IL)-8, IL-6, and intercellular adhesion molecule-1 (ICAM-1) were determined by real-time polymerase chain reaction. Results: A. actinomycetemcomitans facilitated the mRNA expression of MMP-3, IL-8, IL-6, and ICAM-1 in HGECs, whereas these mRNA levels were attenuated by the H. cordata treatment. In addition, the extracellular signal-regulated kinase (ERK) signaling cascade, which was reported to be involved in A. actinomycetemcomitans-induced increases in MMP-3, IL-8, or ICAM-I, was disturbed by the H. cordata treatment in HGECs. Furthermore, H. cordata also inhibited the tumor necrosis factor-alpha-induced enhancement in these genes in HGECs. Conclusion: These results suggest that H. cordata suppresses the expression of inflammatory-related genes in gingival epithelial cells by inhibiting the ERK signaling cascade. This might result in the suppression of inflammatory response in gingival epithelium, thereby contributing to the prevention of periodontitis. Copyright (C) 2014, Association for Dental Sciences of the Republic of China. Published by Elsevier Taiwan LLC. All rights reserved.