An Andrographis paniculata Burm. Nees extract standardized for three main Andrographolides prevents house dust mite-induced airway inflammation, remodeling, and hyperreactivity by regulating Th1/Th2 gene expression in mice.

ETHNOPHARMACOLOGICAL RELEVANCE

Andrographis paniculata Burm. Nees (AP) is an herb used traditionally in Indian and Chinese traditional medicine for the treatment of various inflammatory and respiratory tract diseases. However, the anti-inflammatory potential of standardized Andrographis paniculata 50% ethanol extract (APEE) in the murine model of asthma has not been investigated.

AIM OF THE STUDY

This study aimed to evaluate the protective anti-inflammatory potential and better understand the underlying mechanism of action of APEE in a clinically-relevant mouse asthma model. Thereafter, develop the ethanolic extract of AP as a supplement for asthma prophylaxis.

MATERIALS AND METHOD

APEE was prepared and standardized for AGP, NAG, and DDAG using a high-performance liquid chromatography system. Asthma was induced according to a 14-day house dust mite (HDM) induction protocol. The prophylactic potential of APEE (50 mg/kg - 200 mg/kg) was determined by assessing cardinal asthma features, which included BALF leukocyte and differential cell count, BALF cytokine assay, histology, gene expression, and airway hyperreactivity study.

RESULTS

APEE significantly inhibited HDM-induced airway eosinophilia and neutrophilia. In addition to decreased levels of IL-4, IL-5, IL-13, and eotaxin in bronchoalveolar fluid, APEE abrogated HDM-induced airway mucus over-secretion and airway hyper-responsiveness. Administration of APEE downregulated HDM-induced upregulation of the oxidative stress enzyme Duox1 (dual oxidase 1) and marginally induced Nfe2l2 (nuclear factor erythroid 2-related factor 2) gene expressions. Similarly, Th2-related (Serpinb2, Clca3a1, Il4 and Il13) and Muc5ac gene expression were significantly downregulated.

CONCLUSION

Prophylactic administration of APEE prevented the progression of HDM-induced asthmatic responses by down-regulating Th2 cytokine gene expression and oxidative stress level.