ArticleIndian journal of pediatrics2011
Role of vasoactive intestinal peptide in hyperoxia-induced injury of primary type II alveolar epithelial cells.
Article in Indian journal of pediatrics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 6 citations in OpenAlex.
- VIP/PACAP signaling as an alternative target during hyperoxic exposure in preterm newborns.Physiological research · 2021Review
- Prevention of hyperoxia-induced bronchial hyperreactivity by sildenafil and vasoactive intestinal peptide: impact of preserved lung function and structure.Respiratory research · 2014Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveWe investigated the effect of VIP on primary type II alveolar epithelial cells (AECIIs) upon the exposure of hyperoxia.
methodsAECIIs 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.
resultsCell 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.
conclusionsVIP 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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Registered trials
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