RESUMO
Objective: To investigate the effect of adiponectin levels with its related mechanism in diabetic myocardial ischemia-reperfusion injury and ischemia post-conditioning in experimental rats. Methods: A total of 80 male SD rats were randomly divided into 6 groups: Normal sham (NS) group,n=8, Normal ischemia-reperfusion injury (NIRI) group,n=16, Normal ischemia post-conditioning (NIPO) group,n=16 and Diabetic mellitus sham (DMS) group,n=8, Diabetic mellitus ischemia-reperfusion injury (DMIRI) group,n=16, Diabetic mellitus ischemic post-conditioning (DMIPO) group,n=16. DM rats model was established by intraperitoneal injection of streptozotocin; IR model was established by occlusion of left anterior descending (LAD) coronary artery for 30 min followed by reperfusion for 120min; IPO model was established by 3 cycles of ischemia for 10s and reperfusion for10s; the rats in Sham group received silk line wrapping of LAD without occlusion. The myocardial infarction (MI) area was measured by TTC staining, plasma adiponectin level was examined by ELISA, the protein expressions of p-Akt and total-Akt were detected by Western blot analysis. Results: Compared with NIRI group, NIPO group had decreased MI area,P<0.05, while DMIRI group and DMIPO group had increased MI area,P<0.01; compared with NS group, NIRI group and NIPO group showed up-regulated expression of adiponectin and p-Akt,P<0.05 and DMS group showed down-regulated p-Akt,P<0.05. Compared with NIPO group, three DM groups presented down-regulated adiponectin and p-Akt,P<0.05. Linear correlation analysis indicated that plasma adiponectin expression level was negatively related to MI area and positively related to myocardial tissue p-Akt expression with the correlation coefifcient at 0.63 and 0.65 respectively, P<0.01. Conclusion: Down-regulated plasma adiponectin expression may cause the inactivation of PI3K/Akt signal pathway and therefore aggravate DM ischemia-reperfusion injury which cannot be protected by ischemic post-conditioning in experimental rats.
RESUMO
OBJECTIVE To study the Pseudomonas aeruginosas drug resistance in intensive care unit and its fluoroquinolone-resistant molecular mechanism,and provide scientific basis for rational employment of antibiotics in clinic. METHODS E test was used to determine the minimal inhibitory concentrations(MIC) of 13 antibiotics against 83 P. aeruginosa strains. Twenty-eight fluoroquinolone-resistant strains were selected with standard sensitive strain-ATCC27853 as control. The quinolone resistance-determining region(QRDR)of the gyrA and parC genes was amplified by PCR and sequenced. RESULTS The positive rate of P. aeruginosa in sputum specimen was the highest from 83 strains (71.08%). gyrA Genes of all resistant strains had an ACC to ATC mutation in codon 83,leading to the amino acid substitution of threonine for a an isoleucine and 11 high level resistant strains also showed a GAC to GGC mutation in codon 87,leading to the substitution of an aspartic acid a glycine for. In addition,14 resistant strains also had an TCG to TTG mutation in codon 87 of parC gene,leading to the amino acid substitution of a serine for a leucine. We didn't find parC gene mutation existing independent in fluoroquinolone-resistant P. aeruginosa. CONCLUSIONS Meropenem remains highly active against P. aeruginosa. But the abuse of imipenem and other fluoroquinolones leads to rise in their drug-resistance rate. Fluoroquinolone-resistance has increased rapidly,the mechanism of resistance is gene mutant. It displayed that gyrA and parC gene mutation is associated with fluoroquinolone resistance.