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Objective To assess the effect of Tanreqing injection on airway inflammation in rats. Methods A rat model of airway inflammation was generated with lipopolysaccharide (LPS). Tanreqing injection was given by intratracheal instillation, and bronchoalveolar lavage fluid (BALF) from the right lung was collected. BALF total cell and neutrophil counts were then determined. In addition, BALF levels of inflammatory cytokines interleukin-1β, cytokine-induced neutrophil chemoattractant-1 (CINC-1), and tumor necrosis factor-α were measured using enzyme linked immunosorbent assay (ELISA). The middle lobe of the right lung was stained with hematoxylin-eosin and histological changes examined. Results LPS increased airway inflammation, decreased BALF inflammatory cell count, inflammatory cytokine levels, and suppressed leukocyte influx of the lung. The LPS-induced airway inflammation peaked at 24 h, decreased beginning at 48 h, and had decreased markedly by 96 h. Conclusion Tanreqing injection contains anti-inflammatory properties, and inhibits airway inflammation in a dose-dependent manner.

Extralobar pulmonary sequestrations (ELS) are most commonly found within the left thoracic cavity. We report the case of a 10-year-old girl with ELS in the right thoracic cavity, associated with esophageal fistula. Chest computed tomography scans revealed a parenchymal mass between the right lower lobe and the diaphragm. At last, successful resection of the mass and repair of the esophageal fistula were performed. The girl recovered uneventfully.

Background Radiocontrast nephropathy (RCN) is a major complication after radiographic examination. The precise mechanisms underlying RCN are not well understood. Renal tubular cell apoptosis is a feature of RCN, but hyperosmolality cannot fully explain the cytotoxicity of contrast media. There is accumulating evidence that reactive oxygen species (ROS) is involved in the pathophysiology of RCN, whereas the correlation between oxidative stress and contrast media-induced cell apoptosis is not clear. We hypothesized that ROS mediated apoptosis in renal tubular cells exposed to contrast media. Irbesartan, a selective AT1 receptor antagonist has been demonstrated an antioxidative effect. The present study was designed to determine whether irbesartan attenuated the contrast media-induced renal tubular cell apoptosis. Methods NRK-52E cells were exposed to increasing concentration (25, 50, 100, 150 mg iodine mL−1, 335, 384, 420, 521 mOsm kg−1) of ioversol (a non-ionic contrast media) for 1 h or incubated in ioversol (100 mg iodine mL−1, 420 mOsm kg−1) for 15 min, 30 min, 60 min, 120 min, 240 min, respectively. Mannitol with the same osmolality as ioversol (420 mOsm kg−1) also treated NRK-52E cells for 1 h. In separate experiment, irbesartan (0.01, 0.1, 1 mmol L−1) was added 1 h before incubation with ioversol (100 mg iodine mL−1, 420 mOsm kg−1) for 1 h. Apoptosis was determined by Hoechst staining and flow cytometry with annexinV-FITC and propidium iodide. The intracellular formation of ROS was detected by confocal microscopy with fluorescent probe CM-H2DCFDA. Bax and bcl-2 mRNA expression were determined by reverse transcription–polymerase chain reaction (RT–PCR). Results Ioversol induced NRK-52E cells apoptosis in a concentration- and time-dependent manner. The intracellular ROS generation was greatly increased following ioversol stimulus. Furthermore, ioversol induced a decrease in the expression for bcl-2 mRNA and an increase for bax mRNA. Irbesartan attenuated the ioversol-induced apoptosis in NRK-52E cells in a dose-dependent manner, in which the protective effect of irbesartan was dependent on decreasing intracellular ROS formation. In addition, irbesartan reversed the ioversol-induced increase in bax mRNA and decrease in bcl-2 mRNA. Conclusion Ioversol induced NRK-52E cells apoptosis in a concentration- and time-dependant manner via an increase in oxidative stress and subsequent to the increase in mRNA expression for bax and reduction in bcl-2 mRNA. Irbesartan attenuated the ioversol-induced apoptosis in NRK-52E cells by reducing oxidative stress and reversing the enhancement of bax mRNA and the reduction in bcl-2 mRNA.