ABSTRACT
Gallibacterium anatis,a member of the Pasteurellaceae family,constitutes a part of the normal micro-flora of the upper respiratory tract and the lower genital tract in chickens.However,increasing evidence indicate that G.anatis is also associated with a wide range of pathological changes,particularly in the reproductive organs,which leads to decreased egg production,lowered animal welfare and increased mortality.As a recently defined opportunistic pathogen limited focus has been placed on the pathogenesis and putative virulence factors permitting G.anatis to cause disease.One of the most studied virulence determinants is a large RTX-like toxin (GtxA),which has been demonstrated to induce a strong leukotoxic effect on avian macrophages.A number of fimbria of different sizes and shapes,particularly the F17-1ike fimbriaes,appear to be common in a diverse selection of G.anatis strains.The capsular material expressed possibly involved in serum resistance,metalloproteases capable of degrading immunoglobulins,hemagglutinins,and all factors which may promote biofilm formation are likely linked to the virulence of G.anatis.This review summarized the putative virulence factors described for this bacterium to date.
ABSTRACT
Objective To investigate the effect of silodosin,a selective alpha1 a-adrenoceptor antagonist on a rat model of testosterone-induced benign prostatic hyperplasia (BPH) and its mechanisms.Methods The rats were divided into three groups:control,testosterone-induced BPH,and silodosin +BPH groups.BPH was induced by subcutaneous injection of testosterone [20 mg/(kg · d)] for 4 weeks.Meanwhile silodosin + BPH groups rats were administered silodosin 4 weeks [100 μg/(kg · d)].After 4 weeks,all animals were sacrificed to examine the blood biochemical profiles,prostate volume,weight,histopathological changes,and epidermal growth factor receptor (EGFR) and B-cell chronic lymphocytic leukemia (CLL)/lymphoma 2 (BCL-2) protein expressions.Results Each group showed an increase compared to their initial body weight;however,differences in weight change between groups were not significant (P ＞ 0.05).The BPH group displayed lower glucose levels than the control group.The serum levels of glutamic oxaloacetic transaminase (GOT) and glutamic pyruvic transaminase (GPT) were not significantly different among groups (P ＞ 0.05).The group treated with silodosin showed significantly lesser prostate size and weight than the testosterone-induced BPH group [volume:(0.93 ± 0.14) cm3 vs (1.75 ± 0.15)cm3,P ＜0.01;weight:(0.97 ±0.06)g vs (1.30±0.05)g,P ＜0.01].In addition,silodosin decreased the expressions of EGFR and BCL-2 in prostate tissues (P ＜ 0.05).Conclusions These results suggest that silodosin suppress the development of BPH by inhibiting the expressions of EGFR and BCL-2.
ABSTRACT
AIM:To explore the role of microRNA-181b (miR-181b) in ischemic injury and autophagy pro-tein 5 (Atg5) levels of mice .METHODS:Oxygen-glucose depletion (OGD) model in N2A cells to mimic ischemic in-jury in vitro was established .A middle cerebral artery occlusion ( MCAO) model to mimic ischemic injury in vivo was also induced in mice.The N2A cell apoptosis after OGD was assessed by in situ cell death detection kit.The Atg5 and caspase-9 expressions were determined by Western blotting .Luciferase reporter assay was performed to identify the direct binding of miR-181b with 3’-UTR of Atg5 mRNA.RESULTS:The alteration of miR-181b expression level by transfection with pre-miR-181b or anti-miR-181b significantly affected N2A cell apoptosis (P<0.05).Accordingly, the changes of miR-181b levels significantly altered the protein level of Atg 5 ( P<0.05 ) .Co-transfection of the luciferase reporters with pre-miR-181b or anti-miR-181b resulted in the inhibition or enhancement of the luciferase activities of luciferase expressing plasmid containing 3’-UTR of Atg5 mRNA (P<0.05).In addition, the miR-181b antagonist significantly reduced the cleaved caspase-9 levels in cerebral ischemic cortex of the mice after MCAO ( P<0.05 ) .CONCLUSION: Down-regulation of miR-181b plays an important role in ischemic injury of mice through regulating Atg 5 protein level.