Study summary · research use only
Akebia saponin D attenuates allergic airway inflammation through AMPK activation
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
This study used human lung epithelial BEAS-2B cells and mouse bone marrow-derived mast cells (BMMCs) in vitro, plus an ovalbumin-induced mouse asthma model, to examine Akebia saponin D (ASD), a triterpenoid saponin, on allergic airway inflammation. Cells were pretreated with ASD (50, 100, or 200 μM) or the AMPK activator AICAR (1 mM) before LPS or IL-33 stimulation; mice received ASD (150 or 300 mg/kg) or AICAR (100 mg/kg). The abstract reports ASD and AICAR reduced TNF-α and IL-6 from BEAS-2B cells and IL-13 from BMMCs and increased p-AMPK; AMPK inhibition partly reversed ASD's cytokine suppression. In mice, ASD and AICAR reduced eosinophil, neutrophil, monocyte, and lymphocyte infiltration and TNF-α, IL-6, IL-4, and IL-13, along with lung histopathological changes.
Abstract
Akebia saponin D (ASD) is a bioactive triterpenoid saponin extracted from Dipsacus asper Wall. ex DC.. This study aimed to investigate the effects of ASD on allergic airway inflammation. Human lung epithelial BEAS-2B cells and bone marrow-derived mast cells (BMMCs) were pretreated with ASD (50, 100 and 200 μΜ) and AMPK activator 5-aminoimidazole-4-carboxamide-1-β-D-ribofuranoside (AICAR) (1 mM), and then stimulated with lipopolysaccharide (LPS) or IL-33. Pretreatment with ASD and AICAR significantly inhibited TNF-α and IL-6 production from BEAS-2B cells, and IL-13 production from BMMCs. Moreover, pretreatment with ASD and AICAR significantly increased p-AMPK expression in BEAS-2B cells. Inhibition of AMPK by siRNA and compound C partly abrogated the suppression effect of ASD on TNF-α, IL-6, and IL-13 production. Asthma murine model was induced by ovalbumin (OVA) challenge and treated with ASD (150 and 300 mg/kg) or AICAR (100 mg/kg). Infiltration of eosinophils, neutrophils, monocytes, and lymphocytes, and production of TNF-α, IL-6, IL-4, and IL-13 were attenuated in ASD and AICAR treated mice. Lung histopathological changes were also ameliorated after ASD and AICAR treatment. Additionally, it showed that treatment with ASD and AICAR increased p-AMPK expression in the lung tissues. In conclusion, ASD exhibited protective effects on allergic airway inflammation through the induction of AMPK activation.
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