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Background:Phytoncide is known to have antimicrobial and anti-inflammatory properties. Purpose: This study was carried out to confirm the anti-inflammatory activity of two types of phytoncide extracts from pinecone waste. Methods: We made two types of animal models to evaluate the efficacy, an indomethacin-induced gastroenteritis rat model and a dextran sulfate sodium-induced colitis mouse model. Result: In the gastroenteritis experiment, the expression of induced-nitric oxide synthase (iNOS), a marker for inflammation, decreased in the phytoncide-supplemented groups, and gastric ulcer development was significantly inhibited (p &lt, 0.05). In the colitis experiment, the shortening of the colon length and the iNOS expression were significantly suppressed in the phytoncide-supplemented group (p &lt, 0.05). Conclusions:Through this study, we confirmed that phytoncide can directly inhibit inflammation in digestive organs. Although further research is needed, we conclude that phytoncide has potential anti-inflammatory properties in the digestive tract and can be developed as a functional agent.

For centuries, herbs have been used by traditional therapists around the world to treat gastrointestinal tract disorders, such as gastritis. We hypothesized that the anti-Helicobacter pylori properties of phytoncide, which is extracted from pinecone waste, would facilitate use as a natural gastroprotective product to treat gastrointestinal tract disorders. Thus, we investigated in vitro antibacterial efficacy against H. pylori by agar diffusion assay. To determine the gastroprotective properties of phytoncide, we conducted hematoxylin and eosin staining, performed assays for the detection of the cytotoxin gene, and evaluated pro-inflammatory cytokine expression in H. pylori-infected C57BL/6 mice. Phytoncide significantly inhibited the survival of H. pylori in the gastrointestinal system of C57BL/6 mice. Reduction of gastric severity in H. pylori-infected mice was associated with reductions in the expression levels of pro-inflammatory cytokines in the gastric mucosa, and of the cytotoxin CagA gene in phytoncide treated groups (P P H. pylori in gastro tissue, possibly due to the abundant α-pinene present in the phytoncide as detected by HPLC analysis. Further studies are needed to validate our findings, but we suggest that phytoncide has the potential to be used as a natural ingredient in anti-H. pylori products.

Mastitis is a prevalent inflammatory disease that remains one of the main causes of poor quality of milk. Phytoncides are naturally occurring anti-inflammatory compounds derived from plants and trees. To determine if treatment with phytoncide could decrease the severity of lipopolysaccharide (LPS)-induced inflammatory responses, mammary alveolar epithelial cells (MAC-T) were pretreated with phytoncide (0.02% and 0.04% (v/v)) followed by LPS treatment (1 and 25 μg/ml). The results demonstrated that phytoncide downregulated LPS-induced pro-inflammatory cyclooxygenase-2 (COX-2) expression. Additionally, LPS-induced activation of ERK1/2, p38, and Akt was attenuated by phytoncide. Treatment of cells with known pharmacological inhibitors of ERK1/2 (PD98059), p38 (SB203580), and Akt (LY294002) confirmed the association of these signaling pathways with the observed alterations in COX-2 expression. Moreover, phytoncide attenuated LPS-induced NF-κB activation and superoxide production, and, finally, treatment with phytoncide increased Nrf2 activation. Results suggest that phytoncide can decrease LPS-induced inflammation in MAC-T cells.