Relationship between Notch receptors and hyperoxia-induced lung injury in newborn rats

Author(s):  
Zhang Qianshen ◽  
Chang Liwen ◽  
Liu Hanchu ◽  
Rong Zhihu ◽  
Chen Hongbing
Author(s):  
Chang Liwen ◽  
Rong Zhihui ◽  
Zhang Qianshen ◽  
Qian Liling

1995 ◽  
Vol 4 (6) ◽  
pp. 431-436 ◽  
Author(s):  
M. R. Pierce ◽  
C. A. Voelker ◽  
I. R. S. Sosenko ◽  
S. Bustamante ◽  
S. M. Olister ◽  
...  

We evaluated the effects of sustained perinatal inhibition of NO synthase (NOS) on hyperoxia induced lung injury in newborn rats. NG-nitro-Larginine-methyl-ester (L-NAME) or untreated water was administered to pregnant rats for the final 7 days of gestation and during lactation; followed by postnatal exposure to hyperoxia (>95% O2) or room air. The survival rate of L-NAME treated pups when placed in > 95% O2at birth was significantly lower than controls from day 4 (L-NAME, 87%; control pups, 100%, p < 0.05) to 14 (L-NAME, 0%; control pups, 53%, p < 0.05). Foetal pulmonary artery vasoconstriction was induced by L-NAME with a decrease in internal diameter from 0.88 ± 0.03 mm to 0.64 ± 0.01 mm in controlvs. L-NAME groups (p < 0.05), respectively. We conclude that perinatal NOS inhibition results in pulmonary artery vasoconstriction and a decreased tolerance to hyperoxia induced lung injury in newborn rats.


2018 ◽  
Vol 44 (4-5) ◽  
pp. 226-240 ◽  
Author(s):  
Arben Dedja ◽  
Antonina Gucciardi ◽  
Giuseppe Giordano ◽  
Iole Maria Di Gangi ◽  
Andrea Porzionato ◽  
...  

2001 ◽  
Vol 281 (2) ◽  
pp. L336-L344 ◽  
Author(s):  
Richard L. Auten ◽  
S. Nicholas Mason ◽  
David T. Tanaka ◽  
Karen Welty-Wolf ◽  
Mary H. Whorton

Inflammation may contribute to lung injury and impaired alveolar development in bronchopulmonary dysplasia. We treated hyperoxia-exposed newborn rats with antibodies to the neutrophil chemokine cytokine-induced neutrophil chemoattractant-1 (CINC-1) during 95% O2exposure to reduce adverse effects of hyperoxia-induced inflammation on lung development. Rats were exposed at birth to air, 95% O2, or 95% O2+ anti-CINC-1 (injected on days 3 and 4). Bromodeoxyuridine (BrdU) was injected 6 h before death. Anti-CINC-1 treatment improved weight gain but not survival at day 8. Anti-CINC-1 reduced bronchoalveolar lavage neutrophils at day 8 to levels equal to air controls. Total detectable lung CINC-1 was reduced to air control levels. Lung compliance was improved by anti-CINC-1, achieving air control levels in the 10-μg anti-CINC-1 group. Anti-CINC-1 preserved proliferating cell nuclear antigen expression in airway epithelium despite 95% O2exposure. BrdU incorporation was depressed by hyperoxia but preserved by anti-CINC-1 to levels similar to air control. Alveolar volume and surface density were decreased by hyperoxia but preserved by anti-CINC-1 to levels equal to air control. Blockade of neutrophil influx in newborns may avert early lung injury and avoid alveolar developmental arrest that contributes to bronchopulmonary dysplasia.


1998 ◽  
Vol 125 (7) ◽  
pp. 1455-1462 ◽  
Author(s):  
Anna Radomski ◽  
Grzegorz Sawicki ◽  
David M. Olson ◽  
Marek W. Radomski

2018 ◽  
Author(s):  
Fengdan Xu ◽  
Wenlong Deng ◽  
Xiangyong Kong ◽  
Zhichun Feng

Ulinastatin (UTI) can support protection for several organs through inhibition of the release of inflammatory factors, absorbing oxygen radicals, and inhibition the progression of fibrosis. However, whether UTI has effect on hyperoxia-induced lung injury is still unclear. In this study, the effects of UTI treatment on newborn rats suffering hyperoxia-induced lung injury were examined. The results demonstrated that UTI treatment significantly attenuated the wet/dry weight ratio, downregulated the levels of tumor necrosis factor-α (TNF-α), inhibited macrophage infiltration, and improved the average weight of rats. The most significant changes were observed in high-dose UTI treatment group. However, UTI had no effect on pulmonary superoxide dismutase (SOD) and malondialdehyde (MDA) levels. Our results suggested that Ulinastatin prevents hyperoxia-induced lung injury on newborn rats by downregulating TNF-α and inhibiting macrophage infiltration.


2018 ◽  
Vol 88 (5-6) ◽  
pp. 270-280
Author(s):  
Osman Bastug ◽  
Mehmet Fatih Sonmez ◽  
Mehmet Adnan Ozturk ◽  
Levent Korkmaz ◽  
Hakan Kesici ◽  
...  

Abstract. The aim of this study was to evaluate the therapeutic effect of lycopene on a hyperoxia-induced lung injury model in rat pups. Full-term rat pups were included in the study 12–24 h after delivery. The pups were separated into 4 groups: normoxia control (NC), hyperoxia control (HC), hyperoxia + lycopene (HL), and normoxia lycopene (NL). The normoxia groups were housed in ambient air, and the hyperoxia groups in > 85% O2. HL and NL groups received 50 mg lycopene in oil/kg body weight/day delivered intraperitoneally (i.p.), the other groups received oil alone. On day 11, the rat pups were sacrificed and their lungs removed. Statistically significant injury was observed in all histological parameters measured (MLI, proliferating cell nuclear antigen (PCNA), and apoptosis) in the HC group (HC vs NC, p = 0.001). This injury could not be reversed with lycopene treatment (HC vs HL, 0.05; NC vs HL, p = 0.001). With hyperoxia, statistically significant decreases were observed in biochemical parameters in terms of SOD, MDA, and IL-6 values (HC vs NC: SOD, p = 0.02; MDA, p = 0.043; IL-6, p = 0.001). The use of lycopene did not provide any improvement in these values (HC vs HL, p > 0.05). Hyperoxia or lycopene had no effect on IL-1β and GPx (p > 0.05). When comparing NC and NL groups, negative effects were observed in the group given lycopene in terms of MLI, PCNA, apoptosis, and IL-6 (all parameters, p = 0.001). We observed that 50 mg lycopene in oil/kg body weight/day given via i.p. had no curative effect on the hyperoxia-induced lung injury in newborn rats and may even induce adverse effects.


2016 ◽  
Vol 52 (1) ◽  
pp. 69-76 ◽  
Author(s):  
Mehmet Kose ◽  
Osman Bastug ◽  
Mehmet Fatih Sonmez ◽  
Sedat Per ◽  
Ahmet Ozdemir ◽  
...  

2020 ◽  
Vol 8 (16) ◽  
pp. 1018-1018
Author(s):  
Beibei Jiao ◽  
Yan Tang ◽  
Shan Liu ◽  
Chunyan Guo

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