Background: Cinnamomum camphora (Linn.) Presl has been widely used in traditional Chinese medicine for a variety of purposes. Our previous study indicated the antibacterial mechanism of the essential oil (EO) from C. camphora; however, the anti-inflammatory activity of EO and its underlying mechanism have not been clearly demonstrated. The present study aims to evaluate the anti-inflammatory principle and mechanism of EO.
Methods: The anti-inflammatory activity of EO was evaluated in lipopolysaccharide (LPS)-induced BV2 microglial cells. Nitric oxide (NO) production was measured by NO assay kit. The mRNA expression levels of inducible NO synthase (iNOS), interleukin-6 (IL-6), IL-18 and IL-1β were examined by real time-PCR (RT-PCR). The secretion of pro-inflammatory cytokines in cell supernatants, including IL-6, IL-18 and IL-1β, were assessed by ELISA kits. Furthermore, the metabolic profile of BV2 microglial cells treated with or without EO was explored by GC-MS-based metabolomics analysis. Phosphofructokinase (PFK) and pyruvate kinase (PK) activities were detected by commercial kits.
Results: EO significantly decreased the release of NO and the mRNA expression of iNOS in LPS-induced BV2 microglial cells. EO also attenuated LPS-induced increase in the mRNA expression and secretion of inflammatory cytokines including IL-6, IL-18 and IL-1β. 39 metabolites were identified with significantly different contents, including 21 upregulated and 18 downregulated ones, in the metabolomics analysis. Five pathways were enriched by shared differential metabolites. Additionally, compared with the control group, the glucose level was decreased, while the lactate level was increased, in the culture supernatant of LPS-induced BV2 microglia cells, which were reversed by EO treatment. Besides, compared to the LPS-treated group, the activities for PK and PFK in EO group were decreased by 17.59% and 18.23%, respectively.
Conclusions: The EO from C. camphora acts as an anti-inflammatory agent, which might be mediated through attenuating the glycolysis capacity of microglial cells.