Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242706 (hyperoxia)
 5,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of ascorbic acid on cell size and ascorbic acid transport was studied in hyperoxic astrocytes. Subcultured rat astrocytes plated on poly-L-lysine-coated coverslips or on plastic dishes were exposed to serum-free culture medium and 20% or 42% ambient oxygen for 48 h. Vehicle (homocysteine) or L-ascorbic acid was added to the medium at 0 and 24 h. Cell size and relative optical density of glial fibrillary acidic protein-positive astrocytes were measured by a computerized imaging system. Cells on the dishes were used for ascorbic acid transport studies. Hyperoxia significantly increased the cell size of astrocytes, and this effect was inhibited by ascorbic acid. The rate of L-[14C]ascorbic acid Na(+)-dependent uptake was also inhibited by hyperoxia in vehicle-treated cultures but not in ascorbic acid-supplemented cultures. These results indicate that the presence of ascorbic acid during the hyperoxic episode can prevent astrocytic cell swelling and preserve membrane transport function.
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PMID:Effect of ascorbic acid on hyperoxic rat astrocytes. 873 9

BACKGROUND Lung alveolar epithelial type II cells (AEC II) are the most important stem cells in lung tissues, which are critical for wound repair of bronchopulmonary dysplasia (BPD). This study investigated the effects of calcitonin gene-related peptide (CGRP) on AEC II cells exposed to hyperoxia. MATERIAL AND METHODS Neonatal rat AEC II cells were isolated and identified by detecting surfactant protein C (SP-C). Three small interfering RNAs targeting Notch 1 were synthesized and transfected into AEC II. A hyperoxia-exposed AEC II cell injury model was established and was divided into 8 groups. MDA levels and SOD activity were examined using lipid peroxidation assay kits. Apoptosis and reactive oxygen species (ROS) production were evaluated using flow cytometry. Notch 1 mRNA expression was examined using RT-PCR. Homocysteine-induced endoplasmic reticulum protein (HERP) was examined using Western blot analysis. RESULTS CGRP treatment significantly enhanced MDA levels and decreased SOD activity compared to hyperoxia-treated AEC II cells (P<0.05). CGRP treatment significantly inhibited hyperoxia-induced AEC II cell apoptosis, and significantly suppressed hyperoxia-induced ROS production compared to hyperoxia-treated AEC II cells (P<0.05) either undergoing g secretase inhibitor or Notch RNA interference. CGRP significantly triggered Notch 1 mRNA expression and significantly enhanced HERP expression compared to hyperoxia-treated AEC II cells (P<0.05) either undergoing g secretase inhibitor or Notch RNA interference. CONCLUSIONS In AEC II cells, extrinsic peptide CGRP suppressed hyperoxia-induced apoptosis, oxidative stress, and ROS production, which may be triggered by Notch 1 and HERP signaling pathway.
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PMID:Extrinsic Calcitonin Gene-Related Peptide Inhibits Hyperoxia-Induced Alveolar Epithelial Type II Cells Apoptosis, Oxidative Stress, and Reactive Oxygen Species (ROS) Production by Enhancing Notch 1 and Homocysteine-Induced Endoplasmic Reticulum Protein (HERP) Expression. 2920 8