Flurbiprofen axetil preconditioning allivates inhalation lung injury in rats / 第二军医大学学报

Objective To investigate the protective effects of flurbiprofen axetil(FA) on inhalation lung injury induced by lipopolysaccharides(LPS)inhalation in rats, so as to provide evidence for applying FA in treating inhalation lung injury in clinic. Methods A total of 96 adult male Sprague-Dawley rats were evenly randomized into four groups(n=24): saline negative control group(NS group), model group(LPS group), lipid emulsion preconditioning control group(Lip+LPS group), and FA preconditioning group(FA+LPS group). The model of inhalation lung injury was established with endotracheal instillation of LPS(1 mL/kg)in all experimental groups. NS group was identical to the other three groups except that saline(1 mL/kg)was administered instead of LPS. Lipid emulsion(20%,1 mL/kg)or FA injection(1 mL/kg,10 mg/mL)was intravenously injected via vena caudalis 1 hour before LPS in Lip+LPS and FA+LPS groups, respectively. Rats were sacrificed at 1 h, 6 h, 12 h and 24 h after LPS injection and assigned to 1 h, 6 h, 12 h and 24 h subgroups(n＝6). The arterial blood gas was analyzed and the lungs were removed for determination of the wet/dry mass(W/D)ratio and evaluation of histological injury in all groups. Real-time PCR was used to detect the mRNA levels of PPAR-α and PPAR-γ in rats lung homogenates. The concentration of tumor necrosis factor-alpha(TNF-α)in rat serum was determined by ELISA. Results The rats in LPS and Lip+LPS groups showed damaged structure of lung tissue and inflammation. The mRNA levels of PPAR-α and PPAR-γ in the lung tissues of LPS group were significantly lower than those of NS group(P< 0.05). The serum concentration of TNF-α of LPS group was significantly higher than that of NS group (P<.05). The pulmonary lesions in FA+LPS group were ameliorated compared with those in LPS and Lip+LPS groups. Pressure of oxygen in arterial blood(PaO2)was signficantly higher and semi-quantitative pathological score of lung was signficanlty lower in FA+LPS group than those in LPS and Lip+LPS group at 6 h, 12 h and 24 h after injection(P< 0.05). The mRNA levels of PPAR-α and PPAR-γ in rat lung tissues of FA+LPS group were signficanlty higher than those of LPS and Lip+LPS groups at all times, especially, at 6 h after the intravenous injection of LPS(P< 0.05). The serum concentration of TNF-α of FA+LPS group was significantly lower than that of LPS and Lip+LPS groups at all times, expecially, at 1 h after the intravenous injection of LPS (P<.05). Conclusion FA preconditioning can alleviate the inflammation and protect inhalation injury to lung tissues induced by LPS in rats, which may involve the up-regulation of PPAR-α andPPAR-γ mRNA levels in rat lung tissues and the down-regulation of serum TNF-α.

Increased expression of KCTD9, a novel potassium channel related gene, correlates with disease severity in patients with viral hepatitis B / 中华肝脏病杂志

<p><b>OBJECTIVE</b>Studies have shown that potassium channel plays a pivotal role in T cell activation. The expression of potassium channel gene KCTD9 was evidenced being highly upregulated in patients with severe hepatitis B (SHB). To understand this phenomenon further, tissue and cellular expression profiles of KCTD9 were investigated in patients with SHB.</p><p><b>METHODS</b>A rabbit peptide polyclonal antibody was prepared. Various samples including peripheral blood mononuclear cells (PBMCs); livers from patients with SHB or mild chronic hepatitis B, were examined for KCTD9 expression by quantitative real time PCR and immunohistochemistry staining (IHC). Confocal microscopy was used to illustrate the localizations of the expressions.</p><p><b>RESULTS</b>Increased expression of KCTD9 was observed in PBMC in over 35.7% of the patients with SHB when compared with that of patients with mild chronic hepatitis B. In all patients, the relative value of increased KCTD9 mRNA was positively correlated with alanine aminotransferase, aspartate aminotransferase, total bilirubin and direct bilirubin but negatively with serum albumin. The expression was mainly located in hepatocytes, bile duct epithelial cells, Kupffer cells and inflammatory cells, and in the cytoplasm of PBMCs from the healthy individuals and patients with mild chronic hepatitis B, whereas in both cytoplasm and nuclei in those from patients with SHB.</p><p><b>CONCLUSION</b>The increased expression of potassium channel gene KCTD9 correlates with disease severity in patients with viral hepatitis B.</p>

Effect of puerarin and ligustrazine on cultured hippocampal neurons injury induced by Abeta25-35 / 中国中药杂志

<p><b>OBJECTIVE</b>To investigate the changes of MDA, SOD, LDH of cultured hippocampal neurons injury induced by amyloid-beta protein (Abeta 25-35) and the protective effect of puerarin and ligustrazine.</p><p><b>METHOD</b>Primary hippocampal neurons were cultured and induced by Abeta 25-35. The concentrations of MDA, SOD and LDH in cultured hippocampal neurons were measured after exposed to Abeta 25-35, puerarin and ligustrazine.</p><p><b>RESULT</b>The Alzheimer disease (AD) model was successfully established in cultured hippocampal neurons. AD group has remarkably increased MDA and LDH level, and decreased SOD level, Piracetan group and combined application group of have remarkably decreased MDA and LDH level and increased SOD level, compared with AD group (P < 0.01). Ligustrazine together with puerarin group has remarkably decreased MDA and LDH level and increased SOD level, compared with ligustrazine group and puerarin group (P < 0.05).</p><p><b>CONCLUSION</b>Abeta 25-35 can induce cultured hippocampal neurons injury, combined application of ligustrazine, and puerarin can alleviate the injury.</p>