Asthma is a chronic inflammatory
lung disease that causes respiratory difficulties. Black ginseng extract (BGE) has preventative effects on respiratory inflammatory diseases such as
asthma. However, the pharmacological mechanisms behind the
anti-asthmatic activity of BGE remain unknown. To investigate the
anti-asthmatic mechanism of BGE,
phorbol 12-myristate 13-acetate plus
ionomycin (PMA/Iono)-stimulated mouse EL4 cells and
ovalbumin (OVA)-induced mice with allergic airway
inflammation were used. Immune cells (eosinophils/macrophages),
interleukin (IL)-4, -5, -13, and serum
immunoglobulin E (
IgE) levels were measured using an
enzyme-linked
immunosorbent assay. Inflammatory cell recruitment and mucus secretion in the lung tissue were estimated.
Protein expression was analyzed via Western blotting, including that of
inducible nitric oxide synthase (iNOS) and the activation of
protein kinase C theta (PKCθ) and its downstream signaling molecules. BGE decreased T helper (Th)2
cytokines, serum
IgE, mucus secretion, and iNOS expression in mice with allergic airway
inflammation, thereby providing a protective effect. Moreover, BGE and its major
ginsenosides inhibited the production of Th2
cytokines in PMA/Iono-stimulated EL4 cells. In EL4 cells, these outcomes were accompanied by the inactivation of PKCθ and its downstream
transcription factors, such as nuclear factor of activated T cells (NFAT),
nuclear factor kappa B (NF-κB), activator of transcription 6 (STAT6), and GATA
binding protein 3 (GATA3), which are involved in allergic airway
inflammation. BGE also inhibited the activation of PKCθ and the abovementioned transcriptional factors in the lung tissue of mice with allergic airway
inflammation. These results highlight the potential of BGE as a useful therapeutic and preventative agent for allergic airway inflammatory diseases such as allergic
asthma.