In conclusion, memantine can effectively ameliorate pulmonary inflammation in CS + LPS-induced COPD in mice via reducing NR-1 and xCT expression, glutamate release, Ca<sup>2+</sup> influx, and the phosphorylation of Erk1/2.
These findings demonstrated that H<sub>2</sub> inhalation could inhibit CS-induced COPD development in mice, which is associated with reduced ERK1/2 and NF-κB-dependent inflammatory responses.
Collectively, these data indicated that ERK1/2-siRNA could attenuate PVR in cigarette smoke-exposed rats, and it may have therapeutic value in the treatment of COPD.
TROP2 expression was also inversely correlated with airflow limitation in patients with COPD (r = -0.53, P < 0.01). pcDNA3.1-TROP2-BCs in vitro exhibited improved proliferation with activation of ERK1/2 phosphorylation signaling pathway.
VEGF production was dependent on phosphorylation of ERK-1,-2 and p38MAPK, as was shown by examining the effects of PD 098059 (10 microM), an inhibitor of the upstream activator of MAPKkinase (MKK)-1, and SB 203580 (10 microM), an inhibitor of p38MAPK; there were no differences between non-smokers, smokers without airflow limitation and smokers with COPD in this respect.