ABSTRACT
In recent years, antibiotic resistance of bacteria has become a global health crisis. Especially, the new class of "superbug" was found in South Asia, which is resistant to almost known antibiotics and causes worldwide alarm. Through the underlying mechanisms of bacterial pathogenecity, the expression of many pathogen virulence factors is regulated by the process of quorum sensing. Screening efficient quorum sensing inhibitors is an especially compelling approach to the future treatment of bacterial infections and antibiotic resistance. This article focuses on bacterial quorum sensing system, quorum sensing screening model for in vitro and evaluation of animal models in vivo, recent research of quorum sensing inhibitors and so on.
Subject(s)
Anti-Bacterial Agents/pharmacology , Bacterial Infections , Drug Resistance, Bacterial , Pseudomonas aeruginosa/physiology , Quorum Sensing/drug effects , Animals , Anti-Bacterial Agents/therapeutic use , Bacterial Infections/drug therapy , Disease Models, Animal , Drugs, Chinese Herbal/pharmacology , Humans , Pseudomonas aeruginosa/drug effects , Pseudomonas aeruginosa/pathogenicity , Quorum Sensing/physiology , Virulence/drug effects , Virulence Factors/metabolismABSTRACT
The gene (alyVI) encoding an alginate lyase of marine bacterium Vibrio sp. QY101, which was isolated from a decaying thallus of Laminaria, was cloned using a strategy of combined degenerate PCR and long range-inverse PCR (LR-IPCR), then sequenced and expressed in Escherichia coli. Gene alyVI was composed of a 1014 bp open reading frame (ORF) encoding 338 amino acid residues. The calculated molecular mass of alyVI product is 38.4 kDa, but a signal peptide is cleaved off, leaving a mature protein of 34 kDa. AlyVI was purified from culture supernatants to electrophoretic homogeneity using affinity chromatography. AlyVI was most active at pH 7.5 and 40 degrees C in the presence of 1 mM ZnCl2. A nine-amino-acid consensus region (YXRESLREM), which was only found in polyguluronate lyases, was also observed in the amino-terminal region of AlyVI. However, AlyVI could degrade both M block and G block. These results indicate that a novel alginate lyase-encoding gene has been cloned.
Subject(s)
Gene Expression , Laminaria/microbiology , Polysaccharide-Lyases/genetics , Polysaccharide-Lyases/metabolism , Vibrio/genetics , Amino Acid Sequence , Base Sequence , Cloning, Molecular , DNA Primers , Escherichia coli/metabolism , Hydrogen-Ion Concentration , Molecular Sequence Data , Pacific Ocean , Plasmids/genetics , Sequence Alignment , Sequence Analysis, DNA , Transformation, BacterialABSTRACT
AIM: To study the effects of prophylene glycol mannate sulfate (PGMS) on monocyte chemoattractant protein-1 (MCP-1) mRNA expression in hyperlipidemic rat aorta and to clarify the molecular mechanism of PGMS for the prevention of atherosclerosis. METHODS: PGMS (37.8 and 75.6 mg.kg-1.d-1, ig) or PGMS (37.8 and 75.6 mg.kg-1.d-1, ig) combined with diethyldithiocarbamate (DDC, an inhibitor of SOD, 200 mg.kg-1 every three days, i.p.) were given to hyperlipidemic rats for three weeks. The MDA content and SOD activity were determined after 12 h of starvation, and MCP-1 mRNA expression in aorta was detected by reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: There was significant decrease (29.46% or 58.40)% of MCP-1 mRNA expression in aortic after the therapy. The SOD activity increased markedly and the MDA content decreased at the same time. After treatment with DDC, the SOD activity was inhibited and the MDA content increased, but with no significant effect on MCP-1 mRNA expression. CONCLUSION: PGMS inhibited MCP-1 mRNA expression with no relation to its effect on decreasing MDA content.
Subject(s)
Aorta, Thoracic/drug effects , Chemokine CCL2/biosynthesis , Gene Expression/drug effects , Hypolipidemic Agents/pharmacology , Propylene Glycols/pharmacology , Animals , Aorta, Thoracic/metabolism , Chemokine CCL2/genetics , Hyperlipidemias/blood , Hyperlipidemias/pathology , Male , Malondialdehyde/blood , Malondialdehyde/metabolism , RNA, Messenger/biosynthesis , RNA, Messenger/drug effects , Random Allocation , Rats , Rats, Wistar , Superoxide Dismutase/blood , Superoxide Dismutase/metabolismABSTRACT
AIM: To study the effect of propylene glycol mannate sulfate (PGMS) on induction of CuZn-SOD. METHODS: Wistar rats were given PGMS p.o. at different doses (0, 18.9, 37.8 and 75.6 mg.kg-1.d) for ten days. Then the rats were sacrificed and the total RNA was extracted from the livers. The total RNA samples were loaded on a 1% agarose gel to detect the quality of total RNA. RT-PCR was applied to study the expression of CuZn-SOD mRNA in rat livers. The amplified products were detected by the 1.5% agarose gel electrophoresis. Simultaneously, the CuZn-SOD activities in rat liver were determined by nitrite method. RESULTS: The total RNA extracted from rat livers was integrated without being decomposed by RNase. The level of CuZn-SOD mRNA of the high-dosage group (75.6 mg.kg-1.d) was higher than that of the control group (0 mg.kg-1.d) (P < 0.01); the CuZn-SOD activities of the high-dosage group were significantly higher than those of the control group (P < 0.001) and the CuZn-SOD activities of the middle- (37.8 mg.kg-1.d) and low-dosage groups (18.9 mg.kg-1.d) were higher than those of the control group (P < 0.01). CONCLUSION: PGMS can increase the CuZn-SOD activities as well as CuZn-SOD on mRNA level. Therefore, it is possible for PGMS to counteract Atherosclerosis (AS) by inducing the expression of CuZn-SOD.
Subject(s)
Liver/drug effects , Propylene Glycols/pharmacology , Superoxide Dismutase/biosynthesis , Animals , Dose-Response Relationship, Drug , Free Radical Scavengers/pharmacology , In Vitro Techniques , Liver/metabolism , Male , RNA, Messenger/biosynthesis , RNA, Messenger/drug effects , RNA, Messenger/genetics , Rats , Rats, Wistar , Superoxide Dismutase/genetics , Superoxide Dismutase/metabolismABSTRACT
AIM: To study the effect of propylene glycol mannate sulfate (PGMS) on blood lipids and lipoprotein lipase in hyperlipidemic rat, and its anti-hyperlipidemic mechanism. METHODS: PGMS was administered ig at different doses (37.8 mg.kg-1.d-1 and 75.6 mg.kg-1.d-1) to hyperlipidemic rats for three weeks and blood serum was obtained after starved 12 h. Total cholesterol (TC), triglyceride (TG), low density lipoprotein cholesterol (LDL-C) and high density lipoprotein cholesterol (HDL-C) were examined. The mRNA expression of lipoprotein lipase (LPL) in liver, spleen and artery was detected by reverse transcription polymerase chain reaction (RT-PCR). RESULTS: PGMS significantly decreased the levels of TC, TG and LDL-C and increased that of HDL-C in hyperlipidemic serum dose-dependently. PGMS was shown to increase the level of LPL mRNA expression, which is related directly to the controlling effects of PGMS on blood lipids. CONCLUSION: PGMS modulated blood lipids by promoting mRNA expression of LPL. This may be one important mechanism of PGMS to modulate blood lipids.
