期刊
NEONATOLOGY
卷 113, 期 4, 页码 339-346出版社
KARGER
DOI: 10.1159/000487220
关键词
Xenon; Premature birth; CLIC4; Lipopolysaccharide; Hypoxia-ischennia; Bcl-2; White matter damage
类别
资金
- Shandong Medical and Health Science and Technology Development Program Study on the neuroprotective effect of xenon on hypoxic ischemic brain damage in neonatal rats
Background: Premature birth is a significant health care burden. Xenon (Xe) is a general anesthetic with neuroprotective effects. Objectives: Here, we investigate the neuroprotective role of Xe in a lipopolysaccharide (LPS)- and hypoxiaischemia (HI)-induced white matter damage (WMD) model. Methods:Three-day-old Sprague-Dawley rats were randomly divided into a sham group (group A, n = 24), an LPS + HI group (group B, n = 24), and an LPS + HI + Xe group (group C, n = 72). The onset of Xe inhalation started at 0, 2, and 5 h in subgroups C1, C2, and C3, respectively. Next, we performed TUNEL and hennatoxylin and eosin (HE) staining; and examined the expression of CLIC4 and Bcl-2 in brain tissues. Results: HE staining revealed distorted cytoarchitecture, tangled nerve fibers, and pyknosis in group B, while Xe treatment improved these histological alterations in the group C pups. Following LPS and HI insult, the number of apoptotic cells significantly increased in group B at 48 and 72 h (p < 0,05), and Xe significantly alleviated apoptosis (p < 0.001) at 24, 48, and 72 h, respectively. Similarly, CLIC4 nnRNA expression was significantly increased in group B (p < 0.05), and Xe produced a marked reduction in CLIC4 nnRNA expression in group C subgroups (p < 0.05). Western blotting demonstrated enhanced Bcl-2 expression in group C when compared to group B (p < 0.05). Conclusions:These results demonstrate that LPS and HI successfully induced WMD, and Xe decreased neuronal apoptosis via Bcl-2- and CLIC4-mediated pathways. Moreover, the therapeutic time window of Xe extended for up to 5 h. These findings suggest that Xe can be used as a protective treatment for WMD in premature infants. (C) 2018 S. Karger AG, Basel
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