ABSTRACT
Objective To investigate the effect of propofol pretreatment on the expression of phosphorylated c-Jun N-terminal kinase (p-JNK), matrix metalloproteinase-9 (MMP-9) and aquaporin-4 (AQP-4) during focal cerebral ischemia-reperfusion (I/R) in rats. Methods Seventy-two healthy male SD rats weighing 250-280 g were randomly divided into 4 groups (n = 18 each): sham operation group (group S), I/R group and propofol pretreatment group (P1 and P2). In group I/R, P1 and P2, focal cerebral I/R was induced by occlusion of middle cerebralartery for 2 h followed by 24 h of reperfusion. In group P1 and P2, intraperitioneal 0.5 % and 1% propofol 10 ml/kg were injected 30 rmin before ischemia respectively. In group I/R, normal saline 10 ml/kg was given instead of propofol 30 min before ischemia. Neurological deficit score (NDS) was assessed after consciousness was recovered. 2% Evans blue (EB) 3 ml/kg was injected intravenously 1 h before the animals were sacrificed at 24 h of reperfusion. The brain tissues were taken for determination of the brain water content, EB content and expression of p-JNK, MMP-9 and AQP-4. Results Compared with group S, the NDS and content of water and EB were significantly increased and the expression of p-JNK, MMP-9 and AQP-4 was up-regulated in group I/R, P1 and P2(P ＜ 0.05). Compared with group I/R, the NDS and content of water and EB were significantly decreased and the expression of p-JNK, MMP-9 and AQP-4 was down-regulated in group P1 and P2 (P ＜ 0.05). Compared with group P1 , the expression of p-JNK and MMP-9 was down-regulated (P ＜ 0.05), but no significant difference was found in the NDS, water and EB content and the expression of AQP-4 in group P2 (P ＞ 0.05). Conclusion Propofol pretreatment can reduce focal cerebral I/R injury by inhibiting the activation of JNK signal pathway and up-regulation of MMP-9 and AQP-4 expression.
ABSTRACT
The susceptibility to 9 kinds of antibiotics of 393 animal pathogenic E. coli isolated from clinical samples was determined from 2000 to 2003. The resistance to TC, GM, CMP, AMP, RA, KM, FT, SM and CIP were 93.89%, 57.76%,78.63%, 77.86%, 92.11% ,47.33%, 46.82%, 76.84% and 74.81%, respectively. The isolates could be classified into eight classes according to the number of drugs to which srains were resistant. The resistance spectrum of the isolates varied from 2to 9 kinds of the above drugs. The strains that were resistant to seven kinds of drugs were more than 80 percent. The resistance rates of swine origin strains to GM,AMP and KM were higher than those of poultry origin strains, while the resistance rates of poultry origin strains to TC, CMP, SM and CIP were higher remarkably than those of swine origins. The frequency of resistance increased from 2000 to 2003,which was from 67.33% to 90.58% for CMP, 71.29% to 84.81% for AMP, 73.76%to 80.10% for SM and 61.88% to 88.48% for CIP. At the same time, the resistance rate of GM decreased from 61.39% to 53.92%. Thirty-seven strains (95 %) could make all the Kunming mice die within 72 h injected intraperitoneally with the culmice three times in vivo. The pathogenicity of wild strains with drug resistance acquired naturaly to mice did not decline.
ABSTRACT
0.05),while were significantly increased in the Group G(P0.05) while remarkably increased in the Group G(P