Hyperoxia-induced oxidative stress plays a key role in many
pulmonary diseases. In an earlier study we found the protective effect of the
neuropeptide substance P (SP) on type II alveolar epithelial cells (AECIIs) after
hyperoxia exposure. Then, we investigated
c-Jun N-terminal kinase (C-JNK) signal transduction pathways in AECIIs before and after
hyperoxia exposure. Primary AECIIs were isolated and purified from premature rats. Subsequently, the cells were treated with air (21%
oxygen),
hyperoxia (95%
oxygen), SP+ air, and SP+
hyperoxia. SP was added in advance to reach a final concentration 1 x 10(-6) mol/l. The cells were then exposed to air and
hyperoxia for 12, 24, and 48 h. XTT cell proliferation assay and fluorescence-activated cell sorting (FACS) were employed to detect cell growth and apoptosis. Phosphorylated JNK (p-JNK) levels were measured using Western blot assay. The morphological alteration of AECIIs was observed using a transmission electron microscope (TEM). Compared with the simple
hyperoxia treatment, the cell growth and apoptosis percentage was significantly increased and decreased after adding additional SP. Meanwhile, the reduced levels of p-JNKs could be found after adding SP. Furthermore, the morphological damage of AECIIs was greatly improved. These data suggest that SP can promote AECII proliferation and inhibit apoptosis by suppressing JNK signal pathways after
hyperoxia exposure, which attenuates
hyperoxia-induced oxidative stress damage in AECIIs. It might be a potential
therapy for acute
pulmonary injury under
hyperoxia-induced oxidative stress.