Regulating effect of glycyrrhetinic acid on bronchial asthma smooth muscle proliferation and apoptosis as well as inflammatory factor expression through ERK1/2 signaling pathway.

To study the influence of glycyrrhetinic acid (GA) on bronchial asthma (BA) smooth muscle proliferation and apoptosis as well as inflammatory factor expression and its molecular mechanism. Male SD guinea pigs were selected and made into asthma models, bronchial asthma smooth muscle cells were cultured and divided into BA group, GA group and GA + LM group that were treated with serum-free RPMI1640 culture medium, serum-free RPMI1640 culture medium containing 50 ng/mL glycyrrhetinic acid, serum-free RPMI1640 culture medium containing 50 ng/mL glycyrrhetinic acid and 100 ng/mL LM22B-10 respectively; normal guinea pigs were collected and bronchial smooth muscle cells were cultured as control group. The cell proliferation activity as well as the expression of proliferation and apoptosis genes, inflammatory factors and p-ERK1/2 was determined. Proliferation activity value and mRNA expression of Bcl-2, TNF-α, IL-4, IL-6, YKL-40, protein expression of p-ERK1/2 of airway smooth muscle cell in BA group were significantly higher than those of control group while mRNA expression levels of Bax, caspase-9 as well as caspase-3 were significantly lower than that of control group (P < 0.05); proliferation activity value and mRNA expression of Bcl-2, TNF-α, IL-4, IL-6, YKL-40, protein expression of p-ERK1/2 of airway smooth muscle cell in GA group were significantly lower than those of BA group (P < 0.05) while the mRNA expression levels of Bax, caspase-9 as well as caspase-3 were significantly higher than those of BA group (P < 0.05); proliferation activity value and mRNA expression of Bcl-2, TNF-α, IL-4, IL-6, YKL-40 of airway smooth muscle cell in GA + LM group were significantly higher than those of GA group (P < 0.05) while mRNA expression levels of Bax, caspase-9 as well as caspase-3 were significantly lower that of GA group (P < 0.05). GA can inhibit the proliferation of bronchial smooth muscle cells and reduce the expression of inflammatory factors by inhibiting the phosphorylation of ERK1/2.