3beta-6beta-dihydroxyolean-12-en-27-oic-acid and Asthma

Asthma is a persistent inflammatory disease characterized by airway obstruction and hyperresponsiveness in association with airway inflammation. In the current research, we studied the anti-inflammatory and anti-asthmatic effects of tiarellic acid (TA) isolated from Tiarella polyphylla, based on asthmatic parameters, such as immunoglobulin E (IgE) level, cytokine release, eosinophilia, airway hyperresponsiveness (AHR), reactive oxygen species (ROS) and mucus hypersecretion, in an ovalbumin (OVA)-sensitized/challenged mouse model. TA significantly inhibited increases in IgE, levels of ROS and T helper cytokines, such as interleukin (IL)-4, IL-5, TNF-α, and IL-13, in bronchoalveolar lavage fluid (BALF), and effectively suppressed airway hyperresponsiveness, eosinophilia, and mucus hypersecretion in the asthmatic mouse model. In addition, we found that administration of TA attenuated ovalbumin-induced increases in NF-κB activity in lungs. The efficacy of TA was comparable to that of montelukast, a currently available anti-asthmatic drug. Our results support the utility of TA as a herbal medicine for asthma treatment and may have application in the development of anti-inflammatory and anti-asthmatic drugs.

Topics: Animals; Anti-Asthmatic Agents; Anti-Inflammatory Agents; Asthma; Bronchial Hyperreactivity; Bronchoalveolar Lavage Fluid; Cytokines; Disease Models, Animal; Eosinophilia; Female; Immunoglobulin E; Inflammation; Leukocyte Count; Mice; Mice, Inbred BALB C; Oleanolic Acid; Ovalbumin; Phytotherapy; Transcription Factor RelA; Triterpenes

Bronchial asthma is characterized by chronic lung inflammation, airway hyperresponsiveness (AHR), and airway remodeling. Astilbic acid, extracted from the medicinal herb Astilbe chinensis, is used as a headache remedy in traditional medicine and has anti-pyretic and analgesic effects. However, the effect of astilbic acid on asthma remains to be established. In the present study, we therefore examined the effect of astilbic acid in a mouse model in which asthma was established by sensitization and challenge with ovalbumin (OVA). Astilbic acid inhibited OVA-induced AHR to inhaled methacholine and significantly suppressed the levels of T-helper 2-type cytokines (including IL [interleukin]-4, IL-5, and IL-13) and inflammatory cells (including eosinophils) in bronchoalveolar lavage (BAL) fluid. Histochemical analysis revealed reduced goblet cell hyperplasia and mucus production, as well as attenuated eosinophil-rich leukocyte infiltration, in the astilbic acid-treated group, compared with OVA-challenged mice. Moreover, the compound significantly inhibited synthesis of IL-4-, IL-5-, IL-13-, IL-17-, and eotaxin-encoding mRNA following asthma induction in lung tissue, in addition to suppressing the immunoglobulin E (IgE) response to asthma in both BAL fluid and serum. Our results indicate that astilbic acid has great potential as a therapeutic candidate for the treatment of asthma.

Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Asthma; Bronchoalveolar Lavage Fluid; Cytokines; Disease Models, Animal; Female; Immunoglobulin E; Mice; Mice, Inbred BALB C; Molecular Structure; Oleanolic Acid; Respiratory System; Saxifragaceae; T-Lymphocytes, Helper-Inducer