Related Experiment Video
Updated: Oct 7, 2025
04:27
Intratracheal Instillation of Stem Cells in Term Neonatal Rats
Published on: May 4, 2020
5.8K
Protective Effects of 18β-Glycyrrhetinic Acid on Neonatal Rats with Hyperoxia Exposure
Cai Qing1, Liu Ziyun1, Yu Xuefei1
1Department of Pediatrics, Shengjing Hospital of China Medical University, 36 Sanhao Street, Shenyang, Liaoning, 110004, China.
Inflammation
|January 6, 2022
Summary
18β-Glycyrrhetinic acid (18β-GA), derived from licorice, protects neonatal rats from lung injury caused by oxygen toxicity. This compound reduces oxidative stress and inflammation, improving lung development in premature infants at risk for bronchopulmonary dysplasia.
Area of Science:
- Neonatal physiology and pathology
- Pharmacology and toxicology
- Herbal medicine research
Background:
- Bronchopulmonary dysplasia (BPD) is a severe lung condition in preterm infants, often exacerbated by oxygen therapy.
- Oxygen toxicity induces oxidative stress, inflammation, and impaired lung development, contributing to BPD.
- Licorice extract contains 18β-Glycyrrhetinic acid (18β-GA), known for its antioxidant and anti-inflammatory properties.
Purpose of the Study:
- To investigate the protective effects of 18β-GA against hyperoxia-induced lung injury in neonatal rats.
- To determine if 18β-GA can mitigate oxidative stress and inflammation associated with oxygen toxicity.
- To evaluate the impact of 18β-GA on alveolar development and overall growth in a neonatal rat model.
Main Methods:
- Neonatal Sprague-Dawley rats were exposed to 80% oxygen (hyperoxia) or 21% oxygen (normoxia) from postnatal day 1 to 14.
- Rats received daily intragastric administration of 18β-GA (50 or 100 mg/kg) or vehicle.
- Assessed body weight, alveolar structure, reactive oxygen species (ROS) levels, pulmonary inflammation markers, NF-κB pathway activation, NLRP3 inflammasome, and caspase-1 activity.
Main Results:
- Hyperoxia exposure led to reduced body weight and simplified alveolar structure in neonatal rats.
- Hyperoxia increased ROS levels, pulmonary inflammation, and activated the NF-κB and NLRP3 inflammasome pathways.
- 18β-GA treatment significantly counteracted hyperoxia-induced lung damage by reducing oxidative stress, inflammation, and improving alveolar development and body weight.
Conclusions:
- 18β-GA demonstrates a significant protective effect against hyperoxia-induced lung injury in neonatal rats.
- The therapeutic benefits of 18β-GA are attributed to its ability to inhibit oxidative stress and inflammatory pathways, including NF-κB and NLRP3 inflammasome.
- 18β-GA holds potential as a therapeutic agent to prevent or treat bronchopulmonary dysplasia in premature infants.
