Pinellia polysaccharide activates PI3K/AKT signaling pathway and regulates the expression of airway smooth muscle related apoptosis molecules in airway remodeling in rats with cough variant asthma

Abstract

Purpose: To investigate the effect of Pinellia polysaccharide on airway remodeling in cough-variant asthmatic rats, and the involvement of PI3K/AKT signal route in the process.
 Methods: Seventy-five Sprague-Dawley (SD) rats were assigned to 5 groups: blank control, model, low-dose Pinellia polysaccharide (100 mg/kg), medium-dose Pinellia polysaccharide (200 mg/kg) and high-dose Pinellia polysaccharide (400 mg/kg) groups, each with 15 rats. Immunoblot assay was employed to measure relative protein concentrations of phosphorylated protein kinase B (p-AKT), phosphorylated phosphoinositide-3-kinase (p-PI3K), MMP-9, B lymphocytes expression of cell tumor-2, B-lymphoma-2 gene-related promoter (Bad), Fas, and Caspase-3.
 Results: The levels of Wat, Wam, Wai, p-AKT, p-PI3K, MMP-9 and bcl-2 in model group were significantly higher than those in blank control group (p < 0.05). However, these factors were significantly up-regulated, relative to blank control levels, but lower than those in the model group (p < 0.05). The levels of Bad, Fas and Caspase3 in the model group were significantly lower than the corresponding levels in the blank control group (p < 0.05). Moreover, levels of Bad, Fas and Caspase3 differed significantly amongst rats given the 3 doses of Pinellia polysaccharide (p < 0.05).
 Conclusion: Pinellia polysaccharide mitigates cough-variant asthma in rats through stimulation of PI3K/AKT signal route, regulation of expressions of airway smooth muscle-related apoptotic molecules (Bad, Fas and Caspase-3), and slowing down airway remodeling and airway inflammation. Thus, this polysaccharide is a potential agent for the management of cough variant asthma.