Shenmai Injection （参麦注射液） Inhibiting the Extracellular Signal Regulated Kinase-lnduced Human Airway Smooth Muscle Proliferation in Asthma

Objective： To investigate the relationship between the proliferation of sensitized human airway smooth muscle cells （HASMCs） and the expression of extracellular signal regulated kinase （ERK） and the effect of Shenmai Injection （参麦注射液, SMI） on HASMCs. Methods： The HASMCs cultured in vitro were divided into three groups： （1） control group; （2） sensitized group： containing 10% asthmatic serum; （3） SMI group： further divided into three different concentration subgroups interferred with 10 μL/mL, 50 μL/mL, and 100 μL/mL SMI, respectively. The proliferation of HASMCs was detected using MTT method, the expression of proliferating cell nucleus antigen （PCNA） in HASMCs was detected using immunocytochemical staining, and the expression of phosphoration-ERK1/2 （p-ERK1/2） protein was detected using Western-blot. Results： After passive sensitization, the optical density value （A49o value） of HASMCs was significantly increased from 0.366± 0.086 to 0.839 ± 0.168 （P〈0.05）. In addition, the expression of PCNA was significantly increased from 28.7% ± 5.9% in the control group to 69.8% ±7.5% in the sensitized group （P〈0.05）. At the same time, the expression of p-ERK1/2 in passively sensitized HASMCs was significantly increased compared with the control group （all P〈0.05）. Affer application of 10 μL/mL, 50 μL/mL, and 100 μL/mL SMI to the cultured media of passively sensitized group, the A570 value was significantly decreased from 0.839 ±0.168 to 0.612 ±0.100, 0.412 ± 0.092, and 0.339 ± 0.077, respectively （P〈0.05）. Moreover, the expression of PCNA was significantly decreased from 69.8% ±7.5% to 57.8% ± 6.2%, 40.7%±5.4%, and 26.1% ± 5.2%, respectively. At the same time, the expression of p-ERK1/2 in each SMI group was significantly decreased compared with the sensitized group （all ,P〈0.05）. Conclusion： ERK signal transduction pathway may be involved in the airway remodeling in asthma. The expression of ERK can be inhibited by SMI in a dose-dependent manner, thus preventing the proliferation of HASMCs.