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ROS Plays a Role in the Neonatal Rat Intestinal Barrier Damages Induced by Hyperoxia
D Y Liu1, W J Lou1, D Y Zhang1
1ShengJing Hospital of China Medical University Department of Gastroenterology and Medical Research Center, Liaoning Key Laboratory of Research and Application of Animal Models for Environmental and Metabolic Diseases, SanHao Street #36, HePing District, ShenYang 110000, China.
Insights
Hyperoxia damages neonatal intestinal lining by altering flora and epithelium. N-acetyl-L-cysteine (NAC) protects against this injury, suggesting a role for reactive oxygen species (ROS) in hyperoxia-induced damage.
Area of Science:
- Neonatal physiology
- Gastroenterology
- Cellular biology
Background:
- Hyperoxia is a critical treatment for neonatal illnesses.
- However, hyperoxia can induce intestinal damage in neonatal pups.
- This damage may involve alterations in intestinal flora and mucosal epithelium.
Purpose of the Study:
- To investigate the effects of hyperoxia on intestinal flora and mucosal epithelium in neonatal rats.
- To explore the protective role of N-acetyl-L-cysteine (NAC) against hyperoxia-induced intestinal injury.
- To elucidate the involvement of reactive oxygen species (ROS) in this process.
Main Methods:
- Neonatal rats were exposed to hyperoxia or normoxia.
- Intestinal lavage fluid and tissues were analyzed for biomarkers (D-LA, ET, DAO, i-FABP, L-FABP, cytokines).
- Expression of tight junction proteins (ZO-1, Occludin, Claudin-4) was assessed using immunohistochemistry, western blotting, and RT-PCR. NCM460 cells were used to evaluate NAC's protective effects.
Main Results:
- Hyperoxia significantly increased D-LA, ET, L-FABP, i-FABP, DAO, TNF-α, IL-10, and IFN-γ.
- Hyperoxia decreased the expression of ZO-1, Occludin, and Claudin-4.
- NAC administration promoted cell survival and restored the expression of tight junction proteins, counteracting hyperoxia-induced reductions.
Conclusions:
- Hyperoxia causes significant injury to the intestinal mucosa in neonatal rats.
- Reactive oxygen species (ROS) play a crucial role in mediating hyperoxia-induced intestinal damage.
- N-acetyl-L-cysteine (NAC) demonstrates a protective effect against hyperoxia-induced intestinal injury.
Background:
Hyperoxia treats a subset of critical neonatal illnesses but induces intestinal damage in neonatal pups. In this process, the intestinal flora and mucosal epithelium might be altered by hyperoxia. So the changes of the intestinal flora and mucosal epithelium were studied.
Methods:
Neonatal rats were randomized into the model group that was exposed to hyperoxia and the control group that was maintained under normoxic conditions; then, intestinal lavage fluid and intestinal tissues were harvested. ELISA was used to detect D-lactic acid (D-LA), endotoxin (ET), diamine oxidase (DAO), intestinal fatty acid binding protein (i-FABP), liver-type fatty acid binding protein (L-FABP) and cytokines in the intestinal lavage of neonatal rats during hyperoxia. The intestinal zonula occluden-1 (ZO-1), occlusion protein (Occludin), and closure protein-4 (Claudin-4) of neonatal pups were detected by immunohistochemistry, western blotting, and real-time Polymerase chain reaction (RT-PCR) during hyperoxia. NCM460 cell survival rates were assayed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) during hyperoxia and administration of N-acetyl-L-cysteine (NAC). The expression levels of ZO-1, Occludin, and Claudin-4 in NCM460 cells were detected by immunohistochemistry, western blotting, and RT-PCR during hyperoxia and NAC.
Results:
D-LA, ET, L-FABP, i-FABP, DAO, TNF-α, IL-10, and IFN-γ were significantly increased by hyperoxia, while ZO-1, Occludin, and Claudin-4 were clearly decreased in the hyperoxia group compared with the control group. NAC promoted cell survival, which was inhibited by hyperoxia. The cellular expression levels of ZO-1, Occludin, and Claudin-4, which were lowered by hyperoxia, were increased by NAC.
Conclusion:
Hyperoxia causes injury of the intestinal mucosa, and ROS plays a role in this intestinal damage during hyperoxia.
