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Objective To observe the changes of PPARγ expression in ventilator-induced lung injury rats and explore the role of PPARγ in the pathogenesis of ventilator-induced lung injury. Methods Sixty male Sprague-Dawley rats were randomly divided into 3 groups ( n=21 each ):group N received large tidal volume with mechanical ventilation ( Vt=12 mL/kg);group C received lower tidal volume with mechanical ventilation ( Vt=6 mL/kg);group R received room air without mechanical ventilation. Rats in every group were randomly divided into 3 subgroups respectively by 1,4 and 8 h. The samples of lung were collected at 1,4 and 8 h after ventilation. Lung pathological examina-tion, total protein and white blood cells in bronchoalveolar fluid and wet-to-dry weight were detected. The exoressions of PPARγmRNA were detected by RTPCR;PPARγ protein in lung tissues was detected by western bolt. Result After 4 and 8 h ventilation in group N,total pro-tein and WBC in bronchoalvelor fluid,W/D were markedly higher than those of group C and R (P 0. 05). Conclusion PPARγmRNA and protein expressions in the rats lung tissue of ventilator-induced lung injury were decreased and as-sociated with inflammation and damage of lung tissue.
RESUMO
<p><b>OBJECTIVE</b>To investigate the antagonistic effect and mechanism of the effect of cyproheptadine (Cyp) on endotoxic shock in rats.</p><p><b>METHODS</b>Endotoxic shock was produced in rats by i.v. injection of lipopolysaccharides (LPS) (5 mg/kg). Tumor necrosis factor (TNF(alpha)) mRNA expression was assessed by Northern blot. Plasma TNF(alpha) content was measured by radioimmunoassay. Plasma superoxide dismutase (SOD) activity and malondialdehyde (MDA) content were measured. The intracellular free calcium concentration ([Ca(2+)](i)) in single endothelial cells was determined by laser scanning confocal microscopy (LSCM).</p><p><b>RESULTS</b>Cyp 5 mg/kg injected immediately after i.v. LPS raised the mean arterial blood pressure (MABP) of shocked rats and improved their 24 h survival rate. Meanwhile, Cyp markedly decreased TNF(alpha) mRNA levels in rat liver (18 +/- 10 vs. LPS + saline 38 +/- 10, P < 0.01) as well as plasma TNF(alpha) content [(7.8 +/- 2.4) microg/L vs. LPS + saline (21.5 +/- 3.2) microg/L, P < 0.01)]. It enhanced plasma SOD activity [(1037.2 +/- 112.8) NU/L vs LPS + saline (615.4 +/- 92.6) NU/L, P < 0.01], reduced the MDA content [(5.2 +/- 1.1) micromol/L vs. LPS + saline (9.8 +/- 1.5) micromol/L, P < 0.01], and inhibited TNF(alpha)-induced [Ca(2+)](i) elevation.</p><p><b>CONCLUSION</b>Cyp exerts an anti-endotoxic shock effect by inhibiting TNF(alpha) gene expression, enhancing SOD activity, reducing lipid peroxidation, and preventing [Ca(2+)](i) overload.</p>