Shenmai injection inhibiting the extracellular signal regulated kinase-induced 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 (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 microL/mL, 50 microL/mL, and 100 microL/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 (A A(490) 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). After application of 10 microL/mL, 50 microL/mL, and 100 microL/mL SMI to the cultured media of passively sensitized group, the A(570) 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).


CONCLUSIONS
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.
Zhao
Li-min
LM
Department of Respiratory Diseases, Henan Province People's Hospital, Zhengzhou 450003, China.
Ma
Li-jun
LJ
Zhang
Luo-xian
LX
Wu
Ji-zhen
JZ
D000293:Adolescent; D000328:Adult; D001249:Asthma / Q000201:enzymology* / Q000473:pathology*; D015153:Blotting, Western; D049109:Cell Proliferation / Q000187:drug effects; D004338:Drug Combinations; D004365:Drugs, Chinese Herbal / Q000494:pharmacology*; D048049:Extracellular Signal-Regulated MAP Kinases / Q000037:antagonists & inhibitors* / Q000378:metabolism; D005260:Female; D006801:Humans; D007267:Injections; D008297:Male; D008875:Middle Aged; D032389:Myocytes, Smooth Muscle / Q000187:drug effects / Q000201:enzymology* / Q000473:pathology*; D018809:Proliferating Cell Nuclear Antigen / Q000378:metabolism; D055815:Young Adult
D004338:Drug Combinations; D004365:Drugs, Chinese Herbal; D018809:Proliferating Cell Nuclear Antigen; C009252:fructus schizandrae, radix ginseng, radix ophiopogonis drug combination; D048049:Extracellular Signal-Regulated MAP Kinases