Maternal molecular hydrogen treatment attenuates lipopolysaccharide-induced rat fetal lung injury. (August 2015)

• Record Type: Journal Article
• Authors: Hattori, Y.; Kotani, T.; Tsuda, H.; Mano, Y.; Tu, L.; Li, H.; Hirako, S.; Ushida, T.; Imai, K.; Nakano, T.; Sato, Y.; Miki, R.; Sumigama, S.; Iwase, A.; Toyokuni, S.; Kikkawa, F.
• Is Part Of: Free radical research. Volume 49:Number 8(2015:Aug.)
• Page Start: 1026
• Page End: 1037
• Publication Date: 2015-08
• Subjects: Free radicals (Chemistry) -- Periodicals; Antioxidants -- Periodicals; Vitamin C -- Periodicals; Vitamin E -- Periodicals; 541.224
• DOI: 10.3109/10715762.2015.1038257
• Languages: English
• ISSNs: 1071-5762

Abstract

<abstract> <title>Abstract</title> <p>Maternal inflammation is associated with spontaneous preterm birth and respiratory impairment among premature infants. Recently, molecular hydrogen (H<sub>2</sub>) has been reported to have a suppressive effect on oxidative stress and inflammation. The aim of this study was to evaluate the effects of H<sub>2</sub> on fetal lung injury caused by maternal inflammation. Cell viability and the production of interleukin-6 (IL-6) and reactive oxygen species (ROS) were examined by treatment with lipopolysaccharide (LPS) contained in ordinal or H<sub>2</sub>-rich medium (HM) using a human lung epithelial cell line, A549. Pregnant Sprague Dawley rats were divided into three groups: Control, LPS, and HW + LPS groups. Rats were injected with phosphate-buffered saline (Control) or LPS intraperitoneally (LPS) on gestational day 19 and provided H<sub>2</sub> water (HW) ad libitum for 24 h before LPS injection (HW + LPS). Fetal lung samples were collected on day 20, and the levels of apoptosis, oxidative damage, IL-6, and vascular endothelial growth factor (VEGF) were evaluated using immunohistochemistry. The number of apoptotic cells, and levels of ROS and IL-6 were significantly increased by LPS treatment, and repressed following cultured with HM in A549 cells. In the rat models, the population positive for cleaved caspase-3, 8-hydroxy-2′-deoxyguanosine, IL-6, and VEGF was significantly increased in the LPS group compared with that observed in the Control group and significantly decreased in the HW + LPS group. In this study, LPS administration induced apoptosis and oxidative damage in fetal lung cells that was ameliorated by maternal H<sub>2</sub> intake. Antenatal H<sub>2</sub> administration may decrease the pulmonary mobility associated with inflammation in premature infants.</p> </abstract>