[Modulation of lung oxidant/antioxidant status by ischemic post-conditioning during ischemia/ reperfusion injury: experiment with rats].

OBJECTIVE: To investigate the effects of ischemic post-conditioning (IPO) on the lung endogenous oxidant-antioxidant system and nitric oxide level during the early stage of ischemia/reperfusion (I/R) injury. METHODS: Twenty four male Sprague-Dawley rats were randomly divided into 3 equal groups: sham-operation (S) group, I/R Group, undergoing ischemia by blocking the lung hilus for 1 h and then reperfusion for 30 min, IPO Group, undergoing blocking the lung hilus for 1 h and then 3 cycles of 10 s ischemia and 10 s reperfusion. Then the rats were killed with their lungs taken out. The levels of glutathione (GSH), nitric oxide (NO), malondialdehyde (MDA), xanthine oxidase (XO), and endogenous antioxidant enzymes, i. e, superoxide dismutase (SOD), and catalase (CAT), and activities of gultathionine peroxidase (GPX) and myeloperoxidase (MPO), a neutrophil accumulation marker, were measured respectively. RESULTS: In IPO group, Compared with I/R group, antioxidant systems such as the levels of SOD, CAT, GPX, and GSH of IPO Group were (41.4 +/- 4.4 ) U/mg, (19.5 +/- 1.6) U/mg, (168 +/- 13) U/mg, and (1.72 +/- 0.26) U/g, all significantly higher than those of I/R Group [(19.6 +/- 2.8) U/mg, (8.4 +/- 0.8) U/mg, (72 +/- 8) U/mg, and (0.89 +/-+/- 0.07) mg/g respectively, all P < 0.05); and the levels of XO, MPO, and MDA of Group IPO were (50 +/- 6) U/g, (5.0 +/- 0.5) U/g, and (0.91 +/- 0.08) nmol/mg respectively, all significantly lower than those of I/R Group [(83 +/- 8) U/g, (7.6 +/- 0.7) U/g and (1.58 +/- 0.17) nmol/mg respectively, all P < 0.05). The endogenous NO level of IPO Group was (93 +/- 7) micromol/g, significantly higher than that of I/R Group [(22 +/- 4) micromol/g, P < 0.01]. CONCLUSION: Post-conditioning at onset of reperfusion reduces lung I/R injury. The lung protection of IPO may be mediated, in part, by inhibiting the oxidant generation and oxidizing, and may be associated with the increasing of the endogenous NO level.

Induction of mucin secretion from human bronchial tissue and epithelial cells by rhinovirus and lipopolysaccharide.

AIM: To examine the effects of rhinovirus and lipopolysaccharide (LPS) on mucin secretion from bronchial tissue and epithelial cells in vitro. METHODS: Human small bronchial tissue fragments (HSBTF) and human bronchial epithelial cells (HBEC) were cultured with rhinovirus 16 and LPS, respectively and culture supernatants were collected for mucin measurement. To determine mucin levels in the culture supernatants, a MUC5AC enzyme linked immunosorbent assay and an enzyme linked lectin assay procedure with dolichos biflorus agglutinin (DBA) were developed, and mucin release was expressed as percentage increased (or decreased) secretion over baseline level. RESULTS: A concentration-dependent release of DBA mucin and MUC5AC mucin were observed when HSBTF were infected with various concentrations of rhinovirus 16 at 37 degree. The maximum-induced DBA mucin and MUC5AC mucin release were approximately 258 % and 83 % over baseline. The response of HSBTF to rhinovirus was completely abolished by metabolic inhibitors. Rhinovirus was also able to induce a concentration-dependent release of DBA mucin and MUC5AC mucin from primarily cultured HBEC. LPS 100 mg/L was able to provoke up to approximately 19 % and 54 % increase in DBA and MUC5AC mucin release over baseline, respectively from HSBTF, and 3.1 % and 57 % increase from HBEC at 20 h. Soybean trypsin inhibitor (SBTI) 30 mg/L was able to inhibit LPS-induced mucin release from HSBTF and HBEC. CONCLUSION: Rhinovirus is able to induce mucin secretion from human bronchial tissue and bronchial epithelial cells in vitro. LPS can induce MUC5AC mucin release from HSBTF and HBEC.