Expression and role of anti-oxidative damage factors in the placenta of preterm infants with premature rupture of membranes / 中国当代儿科杂志

OBJECTIVES@#To study the association of the anti-oxidative damage factors nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), and NAD(P)H:quinone oxidoreductase-1 (NQO1) with preterm premature rupture of membranes (PPROM).@*METHODS@#A prospective study was conducted. The neonates who were hospitalized in Yanbian Hospital from 2019 to 2020 were enrolled as subjects, among whom there were 30 infants with PPROM, 32 infants with term premature rupture of membranes (TPROM), and 35 full-term infants without premature rupture of membranes (PROM). Hematoxylin and eosin staining was used to observe the inflammatory changes of placental tissue. Immunohistochemical staining was used to measure the expression of Nrf2, HO-1, and NQO1 in placental tissue. Western blot was used to measure the protein expression levels of Nrf2, HO-1, and NQO1 in placental tissue.@*RESULTS@#Compared with the PPROM group, the TPROM group and the non-PROM full-term group had significantly higher positive expression rates and relative protein expression levels of Nrf2, HO-1, and NQO1 in placental tissue (P<0.05). There were no significant differences in the positive expression rates and relative protein expression levels of Nrf2, HO-1, and NQO1 in placental tissue between the TPROM and non-PROM full-term groups (P>0.05).@*CONCLUSIONS@#The low expression levels of Nrf2, HO-1, and NQO1 in placental tissue may be associated with PPROM, suggesting that anti-oxidative damage is one of the directions to prevent PPROM.

Concerns about neonates discharged against medical advice from the neonatal intensive care unit / 中国当代儿科杂志

Discharge against medical advice (DAMA) conflicts with the purpose of disease treatment in children. Some research has shown that there are high proportions of extremely preterm infants and infants with asphyxia or congenital malformation in neonates with DAMA. This suggests that the sustainable development of neonatology needs cooperation and co-development with obstetrics, neonatal surgery, and radiology to reduce the rate of DAMA. With reference to the current status of research in both China and other countries, this article reviews the causes for DAMA and the strategies for reducing the rate of DAMA, in order to provide a theoretical basis for effectively reducing the rate of DAMA from the neonatal intensive care unit, improving treatment outcomes of the neonates, and increasing hospitals' comprehensive benefits.

Effect of insulin-like growth factor-1 on hyperoxia-induced apoptosis in A549 cells / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To investigate the effect of insulin-like growth factor-1 (IGF-1), which can promote cell differentiation and inhibit cell apoptosis, on hyperoxia-induced apoptosis in A549 cells and its anti-apoptotic mechanism.</p><p><b>METHODS</b>A549 cells were sub-cultured, exposed to hyperoxic conditions and were then treated with different concentrations of IGF-1 (1, 10, and 100 ng/mL) for 48 hours. Cell viability was measured by MTT assay. Cell apoptosis was evaluated by Annexin V-FITC/PI double-staining flow cytometry. Expression levels of Bax and Bcl-2 were measured by flow cytometry.</p><p><b>RESULTS</b>The middle-dose and high-dose IGF-1 intervention groups had higher cell viabilities than the hyperoxic exposure group [(64±3)% and (88±4)% vs (51±3)%; P<0.05]. Compared with the air control group, the hyperoxic exposure group had a significantly higher apoptotic rate [(38.3±5.4)% vs (2.4±0.9)%; P<0.05], a significantly lower expression level of Bcl-2 [(72±5)% vs (91±4)%; P<0.05], and a significantly higher expression level of Bax [(54±6)% vs (3±2)%; P<0.05]. Compared with the hyperoxic exposure group, the low-dose, middle-dose, and high-dose IGF-1 intervention groups had significantly lower apoptotic rates [(16.1±4.7)%, (9.2±2.8)%, and (6.9±2.5)% vs (38.3±5.4)%; P<0.05], significantly higher expression level of Bcl-2 [(79±4)%, (94±4)%, and (100±5)% vs (72±5)%; P<0.05], and significantly lower expression level of Bax [(26±4)%, （5±2)%, and (4±2)% vs (54±6)%; P<0.05].</p><p><b>CONCLUSIONS</b>Hyperoxia significantly inhibits proliferation and promotes apoptosis in A549 cells. IGF-1 may promote cell proliferation and inhibit hyperoxia-induced apoptosis in A549 cells by regulating the expression of Bcl-2 and Bax.</p>

Effects of recombinant human insulin-like growth factor-1 on the expression of Clara cell secretory protein in lung of hyperoxia-exposed newborn rats / 中华儿科杂志

<p><b>OBJECTIVE</b>The development of neonatology and the availability of pulmonary surfactant have been helpful in effective reduction of the mortality of very low birth weight infants at the expense of an increasing number of survivors with bronchopulmonary dysplasia (BPD) caused by lung immaturity. BPD is a common syndrome in newborns, especially in preterm infants, when treated with hyperoxia and mechanical ventilation. Unfortunately, there have been no effective measure for the prevention and treatment of BPD. The purpose of this study was to investigate the influence of recombinant human insulin-like growth factor-1 (rh-IGF-1) on cell apoptosis and Clara cell secretory protein (CCSP) expression during the lung injury induced by hyperoxia, so as to assess its effect on the inflammatory lung injury and its developmental repair.</p><p><b>METHODS</b>Eighty full term neonatal Wistar rats under the same condition were divided randomly into four groups on the second day after birth. Group I was air control, group II was exposed to hyperoxia, group III air + rh-IGF-1, and group IV was treated with hyperoxia + rh-IGF-1. The pups in the control group were kept in room air, while pups in hyperoxia group were kept in a Plexiglas chamber and exposed to over 85% oxygen. Pups in group III were under the same raising condition except for exposure to room air and treated with intraperitoneal injection of rh-IGF-1 (1 microg/Kg) everyday from the third day. Pups in group IV were treated with intraperitoneal injection of rh-IGF-1 (1 microg/Kg) everyday from the third day of exposure to hyperoxia. Lung tissue sections of the neonatal rats were stained with hematoxylin and eosin (HE) after 7 d of hyperoxia exposure, expression of CCSP was examined by immunohistochemical method, and apoptotic cell index of lung tissue was calculated by using TUNEL method.</p><p><b>RESULTS</b>It was observed from immunohistochemical examination that positive staining of CCSP was distributed mainly in distal and respiratory bronchioles. The percentage of Clara cells in distal and respiratory bronchioles epithelium decreased in hyperoxia group (32.17 +/- 3.19)% compared to that in air control group (68.32 +/- 2.04)%, P < 0.01. Statistically significant differences were found in intensity of positiveness of Clara cells between hyperoxia (29.45 +/- 5.56) and air control group (42.37 +/- 3.24), P < 0.01. TUNEL assay showed that most apoptotic cells were alveolar and bronchial epithelial cells. The apoptotic index increased significantly in the hyperoxia group (55.77 +/- 6.09)% compared to the air control group (16.41 +/- 4.01)%, (P < 0.01). The positive rate (52.98 +/- 2.68)% of Clara cells and the expression (41.22 +/- 6.36) of CCSP in hyperoxia + rh-IGF-1 group increased significantly when compared with hyperoxia group, and the differences between these two group were also statistically significant (P < 0.01). The apoptotic index increased significantly in the hyperoxia + rh-IGF-1 group (27.98 +/- 3.09)% compared to the hyperoxia group (P < 0.01).</p><p><b>CONCLUSIONS</b>Hyperoxia exposure can promote the pneumocyte apoptosis and inhibit the expression of CCSP. Rh-IGF-1 can remove the block of the formation of lung alveoli, increase the secretion of CCSP, mitigate inflammatory responses in airway and alleviate lung injury via pneumocyte apoptosis. Therefore, the results of this study provide a theoretic and experimental evidence for clinical application of rh-IGF-1 in prevention and treatment of BPD.</p>

Allergic Pneumonia Animal Model Manufacture / 实用儿科临床杂志

Objective To investigate whether the spores from mushroom antigen can cause the allergic pneumonia and manufacture allergic animal model in the C57BL/_6 mouse.Methods Aged 6 weeks old,weight 25-30 g C57BL/_6 mice were collected.In the mouse tail injection compound of spore antigen and the Freud′s adjuvant.Then pours into through the trachea the antigen once a week.The mice were divided into 4 groups.Group A was the normal mouse,Group B was given Freud′s adjuvant(the same method)to determine whether there was affect to the mouse.Group C and D were injected spore antigen 2 and 4 times.When the antigen sensitization finished 1 week later group C and D were completely divided 2 groups,among them one group was inhalation 1.5% spore antigen and induce the acute response.Six hours later the bronchoalveolar lavage fluid(BALF) was collected to observe cell change,and excise the lung tissue to manufacture the pathology specimen,another group had not been induced the acute response and collect the BALF and to exsise the lung tissue directly.Group B were inhalted saline later to collect the BALF and the lung tissue.In the mouse blood serun,enzyme linked immunosorbent assay(ELISA) was used to mensurate antigen specific IgG.Results In group C and D,antigen specific IgG significantly inhanced than that in group A and B(all P

Protective Effects of Prostaglandin E_1 on Newborn Rats with Hypoxic-ischemic Brain Damage / 实用儿科临床杂志

Objective To study the effect of exogenous prostaglandin E 1 (PGE 1) on the superoxide dismutase(SOD) and nitric oxide(NO) levels in brain tissue of neonatal rats with hypoxic-ischemic brain damage(HIBD).Methods Sixty 7-day old newborn Wistar rats to establish HIBD models,intraperitoneally and subcutaneous injected PGE 1 and TMP,then the rats were killed after hypo- xia and ischemia for 48 hours.Take cerebral cortex of arteria carotis ligation side and made them into homogenate to detect SOD and NO levels in brain tissue.Results SOD level in HIBD group was lower,and NO level was higher than those of normal group(P