RESUMO
One hundred and twenty enterococcal isolates,which were identified from animal specimen,were investigated for the drug-resistance and virulence gene status of Enterococci,so as to provide reference for clinical therapy as well as exploration of Enterococcus pathogenicity.For the 120 Enterococcus isolates,six virulence genes cylA,efaA,Gele,esp,ace and AS were detected with PCR method,and drug-resistance of 11 commonly used antibiotics were measured by K-B disk diffusion tests.The results showed that all of the 120 isolates presented resistance to at least 3 kinds of drugs,and multi-resistance occurred among different originated strains,especially prominent among those isolates from dead swine organs.Generally,the isolates performed highest resistance ratio against lincomycin (115/120),and more than 50 percent isolates were resisted to ciprofloxacin,kanamycin,tetracycline and dalfopristin,while the isolates were least resistant to teicoplanin (1/120).The incidence of cylA,efaA,GelE,esp,ace and AS virulence genes,as a whole,was 39.17％,56.67％,68.33％,23.33％,26.67％ and 13.33％,respectively,but it varied markedly among those of different sources,which showed consistent trend with that drug resistance.It is concluded that the drug-resistance incidence among the test enterococcal isolates showed correlation with that of virulence gene status,and both were closely related to the bacteria origin,therefore,the conventional opportunistic Enterococcus is of value for further exploring these profound relations.
RESUMO
AIM To study the effects of Yizhi Congming Decoction (Ginseng Radix et Rhizoma,Poria,Polygoni multiflori Radix praeparata,etc.) on learning and memory deficits through reducing tau hyperphosphorylation in Aβ-induced AD mice and its mechanism of action.METHODS Sixty ICR mice were randomly and equally assigned into six groups.Sham group (injection of 3 μL normal saline into left hippocampus),model group,donepezil group and each group of Yizhi Congming Decoction (injection of 3 μL Aβ25-35 into left hippocampus).Donepezil group and three treatment groups were gavaged with donepezil and Yizhi Congming Decoction.After 15 days of administration,immunohistochemistry was used to observe the expressions of Ser404 and Thr231.Western blot was performed to evaluate the levels of phosphatidylinositol-3-kinase (PI3K),threonine/serine protein kinase B (AKT) and glycogen synthase kinase 3β (GSK3β).RESULTS Yizhi Congming Decoction attenuated the levels of phosphorylated tau at the Thr231 and Ser404 sites in the hippocampus and increased the phosphorylation levels of PI3K,AKT and GSK3β.CONCLUSION Yizhi Congming Decoction effectively provides protection against learning and memory deficits and inhibits hyperphosphorylated tau protein expression in the hippocampus.The possible mechanism may occur via the PI3 K/Akt-dependent GSK3 β signalling pathway.
RESUMO
AIM To study the effects of Yizhi Congming Decoction (Ginseng Radix et Rhizoma,Poria,Polygoni multiflori Radix praeparata,etc.) on learning and memory deficits through reducing tau hyperphosphorylation in Aβ-induced AD mice and its mechanism of action.METHODS Sixty ICR mice were randomly and equally assigned into six groups.Sham group (injection of 3 μL normal saline into left hippocampus),model group,donepezil group and each group of Yizhi Congming Decoction (injection of 3 μL Aβ25-35 into left hippocampus).Donepezil group and three treatment groups were gavaged with donepezil and Yizhi Congming Decoction.After 15 days of administration,immunohistochemistry was used to observe the expressions of Ser404 and Thr231.Western blot was performed to evaluate the levels of phosphatidylinositol-3-kinase (PI3K),threonine/serine protein kinase B (AKT) and glycogen synthase kinase 3β (GSK3β).RESULTS Yizhi Congming Decoction attenuated the levels of phosphorylated tau at the Thr231 and Ser404 sites in the hippocampus and increased the phosphorylation levels of PI3K,AKT and GSK3β.CONCLUSION Yizhi Congming Decoction effectively provides protection against learning and memory deficits and inhibits hyperphosphorylated tau protein expression in the hippocampus.The possible mechanism may occur via the PI3 K/Akt-dependent GSK3 β signalling pathway.