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Huang B et al. – The 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.
Feng Xu, 10/06/09
| Currently, the role of substance P(SP) in oxidative stress damage is controversial. In present study we found the protective effect of low-dose SP in type II alveolar epithelial cells (AECIIs) under hyperoxia–induced oxidative stress. Also, JNK pathway was suppressed after treatment of SP. It might provide a potential therapy for acute pulmonary injury under hyperoxia-induced oxidative stress. However, we also realize that some issues are needed to be tackled. For exmple, which concentration is optimal for SP to exert its ability against oxidative stress? How AECIIs regulate SP during the period of hyperoxia exposure? Whether other pathways are invovled in after the SP treatment? The questions list above are worthy of investigating in the further study. |
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