PGE1 alleviated alveolar cells apoptosis in rat lung impact injury model / 重庆医学

Objective To investigate the effect of prostaglandin E1 (PGE1)on alveolar cells apoptosis in rat lung impact in-jury model.Methods SD rats were divided into 3 groups (normal control group,lung injury control group and PGE1 treated group).PaO2 and pulmonary coefficient were detected after 24 h of impact.TUNEL labeling was used to evaluate apoptosis and Western blot was used to estimate protein expression levels of beclin-1,LC3 Ⅱ/LC3 Ⅰand NIX.Results After 24 h of impacting, there were obvious structural damage and pneumonedema in rat lung.Compared to normal control group,the PaO2 of lung injury control group decreased and the apoptosis of alveolar cells increased significantly(P <0.05).Furthermore,the expression levels of Beclin-1,LC3Ⅱ/LC3Ⅰ and NIX in the impacting control group were increased (P <0.05 ).In the PGE1 treated group,the PaO2 were decreased compared to normal control group(P <0.05),but these expression levels were higher significantly than lung injury control group (P <0.05).The expression levels of apoptosis,Beclin-1,LC3Ⅱ/LC3Ⅰ and NIX in the PGE1 treated group were in-creased compared to normal control group(P <0.05),but these expression levels were lower significantly than lung injury control group (P <0.05).Conclusion PGE1 could alleviate alveolar cells apoptosis after lung impacting injury,and which effect may as-cribe to PGE1 inhibiting NIX-mediated autophagy and autophagic apoptosis of alveolar cells.

Evaluation of Bronchiolar and Alveolar Cell Injuries Induced by Short- and Long-term Exposure to Sidestream Smoke

BACKGROUND: We investigated effects of short- and long-term exposure to sidestream smoke on the bronchiolar and alveolar cells in Sprague-Dawley rats. METHODS: Rats were divided into five experimental groups: groups 1, 2, and 3 (1-month exposure to 3, 5, and 7 cigarettes a day, respectively), groups 4 and 5 (3- and 6 month exposure to five cigarettes a day, respectively). We examined the morphologic changes, the expressions of tumor necrosis factor alpha (TNF-alpha), tumor growth factor beta1 (TGF-beta1), interlekin (IL)-1alpha, IL-1beta, Ki-67, and cytokeratin 14 and in situ apoptosis in the bronchiolar and alveolar cells on light microscopy (LM) and electron microscopic (EM) terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining. RESULTS: LM showed the respiratory bronchiolar dilatation and alveolar wall collapse. In groups 3, 4, and 5, EM showed loss of the cilia and Clara cells with irregular size, more prominent alveolar wall collapse and dilation of alveolar duct than those of groups 1 and 2. Bronchiolar and alveolar cells showed increased expressions of TNF-alpha and TGF-beta in groups 4 and 5. LM and EM TUNEL stains showed increased apoptosis in groups 3, 4, and 5. CONCLUSIONS: Sidestream smoke causes a bronchiolar and alveolar cell injury and the severity correlates strongly the volume and duration of exposure to sidestream smoke.

The Effects of Nitric Oxide and Sphingosine 1-phosphate on the Pulmonary Microstructure in a Rat Model of Acute Lung Injury: An Intravital Videomicroscopic Approach / 대한흉부외과학회지

BACKGROUND: To evaluate the effects of inhaled nitric oxide (NO) and sphingosine 1-phosphate (S1P) as potential therapeutic agents of acute lung injury, we analyzed the morphology in vivo of the pulmonary microstructure using intravital videomicroscopy in a rat model of acute lung injury. MATERIAL AND METHOD: Sprague Dawley rats were divided into five groups: a control group that underwent normal saline aspiration, an acute lung injury (ALI) group that underwent hydrochloric acid aspiration, and three treatment groups that underwent hydrochloric acid aspiration and were administered therapeutic agents- the S1P group, the NO group, and the S1P+NO group (n=7 per group). To quantify alveolar compliance and interstitial edema, the diameters of all measurable alveoli and interalveolar septa were averaged at one and two hours after aspiration. Alveolar compliance was determined according to diameter changes during the respiratory cycle and the change in tidal volume. RESULT: At two hours after aspiration, the mean alveolar compliance (% change) in the ALI group decreased significantly versus the control group of rats (respiratory cycle: 1.9% for the ALI group vs 6.5% for the control group, p=0.03; tidal volume: 3.2% for the ALI group vs 9.1% for the control group, p=0.003) and versus the NO group (tidal volume: 3.2% for the ALI group vs 16.9% for the NO group, p=0.001). At two hours after aspiration, the mean interalveolar septal thickness in the NO group tended to be smaller as compared to that in the ALI group (15.2micrometer for the ALI group vs 12.3micrometer for the NO group, p=0.06). S1P did not exert a significant effect on the pulmonary microstructure of the injured rat lung. CONCLUSION: Improved alveolar compliance and reduced interstitial edema, observed by intravital videomicroscopy, suggest that inhaled NO ameliorates lung injury.

THE CHANGES AND ITS CLINICAL SIGNIFICANCE OF ULTRASTRUCTURE IN LUNGS OF TYPE 2 DIABETIC PATIENTS / 解剖学报

Objective To investigate the pathological characteristics and clinical significance of ultrasructure in lung tissues of type 2 diabetic adult patients.Methods Normal lung tissues far from lung neoplasm in 10 cases of type 2 diabetic patients associated with lung cancer were observed under a transmission electron microscope. Results Type Ⅱ alveolar cells became small,and cell superficial microvilli disappeared,Osmiophilic lamellar body became atrophy,lacked lamellar structure and formed a solid globule with high electrom dense;Rough endoplasmic reticulum and mitochodria in cytoplasm were enlarged cystiformly,and there were translucent materials deposited in vesicle,euchromatin decreased,heterochromatin condensed;The basement membrane of bronchial capillary were diffusely thickened and mostly showed onion-skin like change,protein deposited around and mixed with basement membrane.Conclusion Lung is confirmed to be the target organ of chronic damage in diabetes.Pathological changes of pulmonary tissues induced by diabetes have its specific characteristics,which are different from other pulmonary diseases.These changes are pathological basis of pulmonary function abnormalities.