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1.
Article in Chinese | WPRIM (Western Pacific) | ID: wpr-347907

ABSTRACT

<p><b>OBJECTIVE</b>Some research has shown that p38 mitogen-activated protein kinase (p38MAPK) plays important roles in lung injuries induced by various factors. Its expression and role in hyperoxia-induced lung injury remains unknown. This study investigated the expression and role of p38MAPK in hyperoxia-induced lung injury juvenile rat model.</p><p><b>METHODS</b>Hyperoxia-induced lung injury rat model was prepared by 90% O(2) exposure. The location and expression of p38MAPK in lung tissues were detected by immunohistochemistry and Western blot respectively. Apoptosis index of lung was evaluated by TUNEL technique. The effect of SB203580, a p38MAPK inhibitor, on the apoptosis index of lung was observed.</p><p><b>RESULTS</b>The expression of phosphor-p38MAPK increased obviously after hyperoxia. Positive phosphor-p38MAPK cells were mainly distributed in the alveolar, airway epithelial cells, pulmonary vascular endothelium cells and infiltrative inflammatory cells. The apoptosis index of lung also significantly elevated. SB203580 inhibited the activation of p38MAPK, and reduced the apoptosis index of lung.</p><p><b>CONCLUSIONS</b>The phosphor-p38MAPK increased and was expressed in many kinds of lung cells in lung injury rat model. It may play a role in the induction of apoptosis in hyperoxia-induced lung injury.</p>


Subject(s)
Animals , Female , Male , Rats , Apoptosis , Disease Models, Animal , Hyperoxia , Imidazoles , Therapeutic Uses , Immunoblotting , Lung Injury , Drug Therapy , MAP Kinase Signaling System , Phosphorylation , Pyridines , Therapeutic Uses , Rats, Wistar , p38 Mitogen-Activated Protein Kinases , Physiology
2.
Article in Chinese | WPRIM (Western Pacific) | ID: wpr-317408

ABSTRACT

<p><b>OBJECTIVE</b>Many studies have shown that tissue development is closely correlated with fluid transport. Aquaporins (AQPs) are a group of cell membrane proteins that actively and selectively transport water. This study aimed to investigate the changes of AQPs expression during lung development in rats in order to elucidate the role of AQPs in the rat lung development.</p><p><b>METHODS</b>AQP1, AQP3, AQP4 and AQP5 proteins and mRNA in the lung cell membrane were measured by immunohistochemistry and reverse transcription-polymerase chain reaction (RT-PCR) respectively in the 20-day-old embryo (E20), 7-day-old newborn rat, and one-month-old young and adult rats. The correlation between AQPs expression and lung development was studied.</p><p><b>RESULTS</b>With increasing age, the lung development showed a dynamic and successive course, with the most rapid from the fetus to the newborn rat, and then a slowed down afterwards. AQPs mRNA was weakly expressed in the lung of the E20 group. Lung AQPs mRNA and protein increased rapidly after birth until adulthood. The AQPs distribution patterns in the lung were unique with no duplication. There was a positive correlation between AQPs expression and lung development (P<0.05).</p><p><b>CONCLUSIONS</b>In addition to being involved in the transepithelial transport of water in the lung, AQPs is also related to its development.</p>


Subject(s)
Animals , Rats , Aquaporins , Genetics , Physiology , Immunohistochemistry , Lung , Embryology , Metabolism , RNA, Messenger , Rats, Wistar
3.
Chinese Journal of Traumatology ; (6): 239-243, 2004.
Article in English | WPRIM (Western Pacific) | ID: wpr-270268

ABSTRACT

<p><b>OBJECTIVE</b>To study the effect of polydatin on phospholipase A(2) in lung tissues in rats with endotoxic shock.</p><p><b>METHODS</b>Thirty-two healthy male Wistar rats were employed in this study. A total of 8 rats received normal saline intravenously (control group), 8 rats received 10 mg/kg of endotoxin (endotoxic shock group), 8 rats received 1 mg/kg of polydatin after endotoxin injection (polydatin treatment group), and 8 rats received 1 mg/kg of polydatin (polydatin prevention group) 30 minutes before endotoxin injection. Mean arterial pressure was measured once half an hour. Lung tissues were collected 6 hours later. Phospholipase A(2) activity was measured with acid titration. The gene expression of secretory phospholipase A(2) type IIA was detected with reverse transcription polymerase chain reaction. Meanwhile, the histological changes of the lungs among four groups were compared through microscopic examination.</p><p><b>RESULTS</b>Phospholipase A(2) activity and the gene expression of secretory phospholipase A(2) type IIA increased after endotoxin injection, but polydatin could inhibit these effects of endotoxin. Obvious morphological evidence could be found in the lung pathological sections and the protective effect of polydatin was most significant in the polydatin prevention group.</p><p><b>CONCLUSIONS</b>Polydatin has prophylactic and therapeutic effects (the former is more distinct than the latter) on acutely injured lungs in rats with endotoxic shock and which suggests that polydatin may be a phospholipase A(2) inhibitor.</p>


Subject(s)
Animals , Male , Rats , Analysis of Variance , Glucosides , Pharmacology , Lung , Metabolism , Phospholipases A , Metabolism , Phospholipases A2 , Rats, Wistar , Reverse Transcriptase Polymerase Chain Reaction , Shock, Septic , Metabolism , Stilbenes , Pharmacology
4.
Article in Chinese | WPRIM (Western Pacific) | ID: wpr-638807

ABSTRACT

Objective To observe the dynamic changes of interferon gamma(IFN-?) and transforming growth factor bata1(TGF-?_1) in animal model of hyperoxia-induced lung injury,and to explore the mechanism of fibrosis.Methods Thirty-two juvenile Wistar rats were randomly divided into room-air group and hyperoxia group,the hyperoxia group were further divided into 3 subgroups of hyperoxia-exposure for 3,7 and 14 days.The mRNA levels of IFN-? and TGF-?_1 in the lung were measured by reverse-transcription polymerase chain reaction(RT-PCR).The expressions of IFN-? and TGF-?_1 protein were measured by immunohistochemical(stai)-ning.Results The level of IFN-? mRNA of groups under hyperxia-exposure for 3,7 and 14 days were higher than that of control group.The expression of IFN-? mRNA notably elevated and was up to its peak(P

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