Abstract

We investigated the effect of VIP on primary type II alveolar epithelial cells (AECIIs) upon the exposure of hyperoxia. AECIIs were isolated and purified from premature rats and exposed to air (21% oxygen), hyperoxia(95% oxygen), VIP+air and VIP+hyperoxia, respectively. The proliferation and apoptosis of AECIIs were detected by MTT cell proliferation assay, flow cytometry and western blot. The production of intracellular reactive oxygen species (ROS) was determined by 2 ', 7'-dichloro-dihydrotestosterone fluorescein diacetate (DCFH-DA) molecular probe and the total antioxidant capacity (TAOC) by ultraviolate spectro-photometer. Cell proliferation significantly increased and apoptosis decreased upon the treatment with VIP. In addition, the level of ROS in the hyperoxia+VIP group was significantly lower than in the hyperoxia group, in contrast, TAOC was higher in the hyperoxia+VIP group than that in the hyperoxia group. VIP exerts a protective role in the hyperoxia-induced oxidative stress damage in AECIIs, which probably attributed to its anti-oxidant and anti-apoptosis property.

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