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\title{18\selectlanguage{greek}β-\selectlanguage{english}Glycyrrhetinic acid protectes neonatal rats with hyperoxia exposure
through inhibiting ROS/NF-\selectlanguage{greek}κ\selectlanguage{english}B/NLRP3 inflammasome\selectlanguage{english}}



\author[1]{Qing Cai}%
\author[1]{Ziyun Liu}%
\author[1]{Xuefei Yu}%
\author[1]{Xinyi Zhao}%
\author[1]{Xindong Xue}%
\author[1]{Jianhua Fu}%
\affil[1]{Shengjing Hospital of China Medical University}%


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  \date{May 20, 2024}


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\begin{abstract}
Bronchopulmonary dysplasia (BPD) is a common devastating pulmonary
complication in preterm infants. Oxygen supplementation is a lifesaving
therapeutic measure used for premature infants with pulmonary
insufficiency. However, oxygen toxicity is a significant trigger for
BPD, and oxidative stress-induced inflammatory responses, in turn,
worsens the oxidative toxicity resulting in lung injury and arresting of
lung development. Glycyrrhiza radix is commonly used in the medicine and
food industries. 18\selectlanguage{greek}β-\selectlanguage{english}Glycyrrhetinic acid (18\selectlanguage{greek}β-\selectlanguage{english}GA), a primary active
ingredient of Glycyrrhiza radix, has a powerful anti-oxidative and
anti-inflammatory effects. This study aimed to determine whether 18\selectlanguage{greek}β-\selectlanguage{english}GA
has protective effects on neonatal rats with hyperoxia exposure. Newborn
Sprague-Dawley rats were kept in either 21\% (normoxia) or 80\% O2
(hyperoxia) continuously from postnatal day (PN) 1 to 14. 18\selectlanguage{greek}β-\selectlanguage{english}GA was
injected intragastrically at 50 or 100 mg/kg body weight once a day from
PN 1 to 14. We examined the body weights and alveolar development, and
measured ROS level and the markers of pulmonary inflammation.
Mature-IL-1\selectlanguage{greek}β \selectlanguage{english}and NF-\selectlanguage{greek}κ\selectlanguage{english}B pathway proteins, and the NLRP3 inflammasome,
were assessed; concurrently, caspase-1 activity was measured. Our
results indicated that hyperoxia resulted in alveolar simplification and
decreased bodyweight of neonatal rats. Hyperoxia exposure increased ROS
level and pulmonary inflammation, and activated NF-\selectlanguage{greek}κ\selectlanguage{english}B and the NLRP3
inflammasome. 18\selectlanguage{greek}β-\selectlanguage{english}GA treatment decreased ROS level, inhibited the
activation of NF-\selectlanguage{greek}κ\selectlanguage{english}B and the NLRP3 inflammasome, decreased pulmonary
inflammation, improved alveolar development, and increased the
bodyweight of neonatal rats with hyperoxia exposure. Our study
demonstrates that 18\selectlanguage{greek}β-\selectlanguage{english}GA protects neonatal rats with hyperoxia exposure
through inhibiting ROS/NF-\selectlanguage{greek}κ\selectlanguage{english}B/NLRP3 inflammasome.%
\end{abstract}%



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\textbf{Hosted file}

\verb`Pediatric Pulmonology.DOCX`  available at \url{https://authorea.com/users/734930/articles/711609-18%CE%B2-glycyrrhetinic-acid-protectes-neonatal-rats-with-hyperoxia-exposure-through-inhibiting-ros-nf-%CE%BAb-nlrp3-inflammasome}

\textbf{Hosted file}

\verb`Table1.docx`  available at \url{https://authorea.com/users/734930/articles/711609-18%CE%B2-glycyrrhetinic-acid-protectes-neonatal-rats-with-hyperoxia-exposure-through-inhibiting-ros-nf-%CE%BAb-nlrp3-inflammasome}

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