Essential Oils of Gardenia jasminoides J. Ellis and Gardenia jasminoides f. longicarpa Z.W. Xie & M. Okada Flowers: Chemical Characterization and Assessment of Anti-Inflammatory Effects in Alveolar Macrophage

Abstract

Alveolar macrophage is the predominant cell type in the lung and is thought to be the major target for anti-inflammatory therapy in chronic obstructive pulmonary disease (COPD). Aromatherapy using natural essential oils with anti-inflammatory effects for inhalable administration is a potential complementary and alternative therapy for COPD treatment. The Gardenia jasminoides flower is famous for its fragrance in East Asia and is used for treating colds and lung problems in folk medicine. Therefore, in the present study, flower essential oils from two main medicinal gardenia varieties (G. jasminoides J. Ellis and G. jasminoides f. longicarpa Z.W. Xie & M. Okada) were extracted by hydro-distillation, and their chemical components were analyzed by GC-MS. The anti-inflammatory effects of the two essential oils and their main ingredients were further studied on lipopolysaccharide (LPS)-induced models in murine alveolar macrophages (MH-S). The results indicated that the chemical constituents of the two gardenia varieties were quite different. Alcohol accounted for 53.8% of the G. jasminoides essential oil, followed by terpenes (16.01%). Terpenes accounted for 34.32% of the G. jasminoides f. longicarpa essential oil, followed by alcohols (19.6%) and esters (13.85%). Both the two gardenia essential oils inhibited the LPS-induced nitric oxide (NO) release and reduced the production of tumor necrosis factor-α (TNF-α) and prostaglandin E2 (PGE2) in the MH-S cells. Linalool and α-farnesene dose-dependently reduced the NO release in the MH-S cells. Linalool and α-farnesene did not affect the PGE2 production but regulated the expression of TNF- α. In addition to linalool and α-farnesene, other components in the gardenia flower essential oils appeared to be able to act as anti-inflammatory agents and influence the PGE2 pathway.