OBJECTIVETo investigate the relationship of the polymorphism of SG13S114A/T in ALOX5AP gene with atherosclerotic cerebral infarction (ACI).

METHODSBy polymerase chain reaction and restriction fragment length polymorphism, polymorphism of SG13S114A/T in ALOX5AP gene in 412 cases with ACI and 368 non-ACI controls were analyzed.

RESULTThere were no statistically significant differences in the ALOX5AP gene SG13S114 AA genotype and A allele frequencies between ACI group and control group (P>0.05).

CONCLUSIONThe results do not support genotype SG13S114 A allele as the risk gene for ACI.control group.

5-Lipoxygenase-Activating Proteins ; genetics ; Alleles ; Cerebral Infarction ; etiology ; genetics ; Female ; Genotype ; Humans ; Intracranial Arteriosclerosis ; complications ; genetics ; Male ; Polymorphism, Restriction Fragment Length

OBJECTIVETo evaluate whether mRNA levels of Pde4d and Alox5ap were associated with hypertensive stroke and hypertension in stroke-prone renovascular hypertensive rats (RHRSP) which could simulate human being's hypertensive cerebral stroke.

METHODSFive groups were established: normotensive group, gradient hypertensive groups I, II and III(with contractive pressure of 140-159 mmHg, 160-179 mmHg and 180-199 mmHg respectively) and spontaneous stroke group. RNA from leukocytes in peripheral blood of each rat underwent real time PCR after reversed.

RESULTSThe mRNA levels of Pde4d and Alox5ap of spontaneous stroke group were statistically higher than that of the other groups. Expression of Pde4d of hypertensive group I was a bit higher than that of normotensive group and hypertensive groups II and III; as for Alox5ap, there was no statistical difference between normotensive group and all gradient hypertensive groups.

CONCLUSIONAnimal experiments come to conclusions that over-expression of Pde4d and Alox5ap are associated with hypertensive stroke but not with hypertension. Therefore, the two genes confer the risk of hypertensive stroke independent of traditional risk factors. It is speculated that over-expression of Pde4d and Alox5ap can motivate onset of hypertensive cerebral stroke by participating in inflammation of arterial walls.

5-Lipoxygenase-Activating Proteins ; Animals ; Carrier Proteins ; genetics ; Cyclic Nucleotide Phosphodiesterases, Type 3 ; genetics ; Cyclic Nucleotide Phosphodiesterases, Type 4 ; Gene Expression Regulation ; Hypertension ; complications ; genetics ; Membrane Proteins ; genetics ; RNA, Messenger ; genetics ; metabolism ; Rats ; Rats, Inbred SHR ; Stroke ; complications ; genetics

OBJECTIVETo investigate the gene expression of MAPEG in the cortex of concanavalin A (Con A)-induced mouse immune inflammatory model and the effect of cyclosporine A (Cs A).

METHODSMale Balb/c mouse immune inflammation model was developed by intravenous injection of Con A (20 mg/kg). Cs A (150 mg/kg) was intravenously infected prior to Con A administration. The MAPEG expressions were determined by RT-PCR.

RESULTmGST1, mGST3, LTC(4)S, FLAP and mPGES-1 were detected by RT-PCR but not mGST2. Eight hours after Con A treatment, mGST1 level was up-regulated to 1.2 approximately 1.5 folds of control with or without Cs A treatment. mGST3ìLTC(4)S, FLAP and mPGES-1 mRNA levels were not influenced by Con A administration.

CONCLUSIONImmune mechanism may be not involved in mGST1 up-regulation in this model and Con A does not alter arachidonic acid metabolism in cortex.

5-Lipoxygenase-Activating Proteins ; Animals ; Brain ; metabolism ; Carrier Proteins ; genetics ; metabolism ; Concanavalin A ; toxicity ; Cyclosporine ; pharmacology ; Eicosanoids ; metabolism ; Glutathione ; metabolism ; Glutathione Transferase ; genetics ; metabolism ; Intramolecular Oxidoreductases ; genetics ; metabolism ; Male ; Membrane Proteins ; genetics ; metabolism ; Mice ; Mice, Inbred BALB C ; Prostaglandin-E Synthases

OBJECTIVETo explore the regularity of recipe composition by observing inhibitory effects on the genic expression of 5-lipoxygenase activating protein, IL-4 and the leukotriene C4 in asthmatic mice.

METHODThe mice were challenged with OVA and administered ig with the Herba Ephedrae decoction (HED), separated compositions (2500 mg x kg(-1), calculated by Herba Ephedrae) and dexamethasone (2 mg x kg(-1)) respectively once daily for seven days. The real-time fluorescence quantitative PCR method was employed to measure the contents of FLAP mRNA and IL-4 mRNA expressions in lung and the ELISA method was used to determine the content of LTC4 in the washing solution of pulmonary alveolus and bronchi.

RESULTIn the lung of asthma mice, the expressions of FLAP and IL-4 and the content of LTC4 were significantly augmented compared with the control group. The HED and the separated compositions could suppress the expressions of FLAP and IL-4 and LTC4 release to a great extent in mice.

CONCLUSIONThe HED had the remarkable effects of antianaphylaxis asthma and the original formula HED worked best. These results confirmed the rationality and scientific level of HED.

5-Lipoxygenase-Activating Proteins ; Animals ; Asthma ; chemically induced ; genetics ; metabolism ; Bronchoalveolar Lavage Fluid ; chemistry ; Carrier Proteins ; biosynthesis ; genetics ; Drugs, Chinese Herbal ; isolation & purification ; pharmacology ; Enzyme-Linked Immunosorbent Assay ; Ephedra sinica ; chemistry ; Interleukin-4 ; biosynthesis ; genetics ; Leukotriene C4 ; metabolism ; Lung ; drug effects ; metabolism ; Male ; Membrane Proteins ; biosynthesis ; genetics ; Mice ; Ovalbumin ; Plants, Medicinal ; chemistry ; RNA, Messenger ; biosynthesis ; genetics ; Random Allocation

OBJECTIVETo investigate the relationship between the polymorphism of SG13S114 A/T in the 5-lipoxygenase-activating protein (ALOX5AP) gene and the stability of carotid atherosclerosis.

METHODSPolymorphism of SG13S114 A/T in the ALOX5AP gene was analyzed in 152 cases of acute infarction with stable plaque, and 132 cases of acute infarction with vulnerable plaques, by using polymerase chain reaction and restriction fragment length polymorphism. Carotid artery plaque was analyzed by carotid artery color ultrasound.

RESULTSThe frequencies of SG13S114 AA genotype and the A allele in the vulnerable plaque group were higher than that in the stable plaque group (P< 0.01).

CONCLUSIONThe polymorphism of SG13S114 A/T in the ALOX5AP gene may be associated with the instability of atherosclerosis. And the SG13S114 A allele may be a risk factor of vulnerable plaques.

5-Lipoxygenase-Activating Proteins ; Aged ; Aged, 80 and over ; Carotid Artery Diseases ; genetics ; Carrier Proteins ; genetics ; Case-Control Studies ; Female ; Gene Frequency ; Genetic Predisposition to Disease ; Genotype ; Humans ; Male ; Membrane Proteins ; genetics ; Middle Aged ; Polymerase Chain Reaction ; Polymorphism, Restriction Fragment Length ; Polymorphism, Single Nucleotide

Chronic myeloid leukemia (CML) is a myeloproliferative disease characterized by the overproduction of granulocytes, which leads to high white blood cell counts and splenomegaly in patients. Based on clinical symptoms and laboratory findings, CML is classified into three clinical phases, often starting with a chronic phase, progressing to an accelerated phase and ultimately ending in a terminal phase called blast crisis. Blast crisis phase of CML is clinically similar to an acute leukemia; in particular, B-cell acute lymphoblastic leukemia (B-ALL) is a severe form of acute leukemia in blast crisis, and there is no effective therapy for it yet. CML is induced by the BCR-ABL oncogene, whose gene product is a BCR-ABL tyrosine kinase. Currently, inhibition of BCR-ABL kinase activity by its kinase inhibitor such as imatinib mesylate (Gleevec) is a major therapeutic strategy for CML. However, the inability of BCR-ABL kinase inhibitors to completely kill leukemia stem cells (LSCs) indicates that these kinase inhibitors are unlikely to cure CML. In addition, drug resistance due to the development of BCRABL mutations occurs before and during treatment of CML with kinase inhibitors. A critical issue to resolve this problem is to fully understand the biology of LSCs, and to identify key genes that play significant roles in survival and self-renewal of LSCs. In this review, we will focus on LSCs in CML by summarizing and discussing available experimental results, including the original studies from our own laboratory.
5-Lipoxygenase-Activating Proteins ; metabolism ; Animals ; Benzamides ; Disease Models, Animal ; Fusion Proteins, bcr-abl ; antagonists & inhibitors ; chemistry ; metabolism ; Humans ; Imatinib Mesylate ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive ; drug therapy ; enzymology ; genetics ; pathology ; Male ; Mice ; Neoplastic Stem Cells ; enzymology ; pathology ; PTEN Phosphohydrolase ; metabolism ; Philadelphia Chromosome ; Piperazines ; therapeutic use ; Point Mutation ; Protein Structure, Tertiary ; Protein-Tyrosine Kinases ; antagonists & inhibitors ; chemistry ; metabolism ; Pyrimidines ; therapeutic use