OBJECTIVE: To interpret the pharmacology of quercetin in treatment of atherosclerosis (AS). METHODS: Fourteen apolipoprotein E-deficient (ApoE^-/-) mice were divided into 2 groups by a random number table: an AS model (ApoE^-/-) group and a quercetin treatment group (7 in each). Seven age-matched C57 mice were used as controls (n=7). Quercetin [20 mg/(kg·d)] was administered to the quercetin group intragastrically for 8 weeks for pharmacodynamic evaluation. Besides morphological observation, the distribution of CD11b, F4/80, sirtuin 1 (Sirt1) and P21 was assayed by immunohistochemistry and immunofluorescence to evaluate macrophage infiltration and tissue senescence. Ultra-performance liquid chromatography/tandem mass spectrometry (UPLC-MSC/MS) was performed to study the pharmacology of quercetin against AS. Then, simultaneous administration of an apelin receptor antagonist (ML221) with quercetin was conducted to verify the possible targets of quercetin. Key proteins in apelin signaling pathway, such as angiotensin domain type 1 receptor-associated proteins (APJ), AMP-activated protein kinase (AMPK), peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α), tissue plasminogen activator (TPA), uncoupling protein 1 (UCP1) and angiotensin II receptor 1 (AT1R), were assayed by Western blot. RESULTS: Quercetin administration decreased lipid deposition in arterial lumen and improved the morphology of ApoE^-/- aortas in vivo. Quercetin decreased the densities of CD11b, F4/80 and P21 in the aorta and increased the level of serum apelin and the densities of APJ and Sirt1 in the aorta in ApoE^-/- mice (all P<0.05). Plasma metabolite profiling identified 118 differential metabolites and showed that quercetin affected mainly glycerophospholipids and fatty acyls. Bioinformatics analysis suggested that the apelin signaling pathway was one of the main pathways. Quercetin treatment increased the protein expressions of APJ, AMPK, PGC-1α, TPA and UCP1, while decreased the AT1R level (all P<0.05). After the apelin pathway was blocked by ML221, the effect of quercetin was abated significantly, confirming that quercetin attenuated AS by modulating the apelin signaling pathway (all P<0.05). CONCLUSION Quercetin alleviated AS lesions by up-regulation the apelin signaling pathway.
Mice ; Animals ; Apelin ; Tissue Plasminogen Activator/metabolism* ; Quercetin/therapeutic use* ; AMP-Activated Protein Kinases/metabolism* ; Sirtuin 1/metabolism* ; Signal Transduction/physiology* ; Atherosclerosis/metabolism* ; Apolipoproteins E

PURPOSE: Dysregulation of adipokines caused by excess adipose tissue has been implicated in the development of obesity-related metabolic diseases. This study evaluated the effects of mugwort (Artemisia princeps Pampanini) ethanol extract on lipid metabolic changes, insulin resistance, adipokine balance, and body fat reduction in obese rats. METHODS: Male Sprague-Dawley rats were fed either a control diet (NC), high-fat diet (HF, 40% kcal from fat), or high-fat diet with 1% mugwort extract (HFM) for 6 weeks. RESULTS: Epididymal and retroperitoneal fat mass increased in the HF group compared with the NC group, and epididymal fat mass was reduced in the HFM group (p < 0.05). No difference was observed in serum levels of total cholesterol (TC) and high-density lipoprotein cholesterol (HDL-C) among the groups. However, triglyceride (TG), TG/HDL-C ratio, and TC/HDL-C ratio increased in the HF group and significantly decreased in the HFM group. TG and TC levels in the liver were significantly higher in the HF group, whereas these levels were significantly reduced in the HFM group. HF rats had lower insulin sensitivity as indicated by increased homeostasis model assessment of the insulin resistance (HOMA-IR) value. HOMA-IR values significantly decreased in the HFM group. Adiponectin levels were higher in NC rats, and their leptin and PAI-1 levels were lower. Relative balance of adipokines was reversed in the HF group, with lower adiponectin levels but higher leptin and PAI-1 levels. In contrast, the HFM group maintained balance of adiponectin/leptin and adiponectin/PAI-1 levels similar to NC by reducing leptin and PAI-1 levels. CONCLUSION: Overall data indicated that mugwort extract can be effective in alleviating metabolic dislipidemia, insulin resistance, and adipokine dysregulation induced by a high-fat diet.
Adipokines* ; Adiponectin ; Adipose Tissue ; Animals ; Artemisia* ; Cholesterol ; Diet ; Diet, High-Fat ; Ethanol ; Homeostasis ; Humans ; Insulin Resistance ; Intra-Abdominal Fat ; Leptin ; Lipid Metabolism ; Lipoproteins ; Liver ; Male ; Metabolic Diseases ; Plasminogen Activator Inhibitor 1 ; Rats* ; Rats, Sprague-Dawley ; Triglycerides

OBJECTIVETo observe the effects of Danhong Injection (丹红注射液) and its main components, including daiclzein and hydroxysafflor yellow A (HSYA), on the anticoagulation, fibrinolysis, anti-apoptosis in hypoxia model of vein endothelial cells (VECs).

METHODSVECs were prepared and were put in a hypoxia environment, which consisted of mixed gas of 95% N and 5% CO mixed gas, when reached confluent culture. Five groups used different treatments, including normal control group, hypoxia group, daiclzein group, HSYA group and Danhong Injection group. The VECs were identified by fluorescence double labeling methods. The morphology was observed by a phase contrast microscopy. The effects of Danhong Injection, daiclzein and HSYA on 6 keto prostaglandin F1α (6-keto-PGF1α) level was measured by the method of radioimmunoassay (RIA). Superoxide dismutase (SOD) activity was tested by water soluble tetrazolium salt. The content of malondialdehyde (MDA) was measured by thiobarbituric acid. The activities of tissue-type plasminogen activator (t-PA) and plasminogen activator inhibitor (PAI) were measured by the method of chromogenic substrate. The contents of endothelin (ET) and nitric oxide (NO) were detected by non-equilibrium RIA and enzymelinked immunosorbent assay. Cells apoptosis rate was determined by flow cytometry.

RESULTSCompared with the normal control group, the floating cells number, PAI activity, ET and MDA contents, and cells apoptosis rate in the culture solution of hypoxia group were all significantly increased, whereas the 6-keto-PGF1α and NO contents, and t-PA and SOD activities were decreased significantly (P<0.01). Compared with the hypoxia group, Danhong Injection markedly increased the 6-keto-PGF1α content and SOD activity, regulated PAI and t-PA activities, ET and NO contents, and decreased MDA content and cells apoptosis rate (P<0.05 or P<0.01).

CONCLUSIONSDanhong Injection and its main components played an important role in protecting primary VECs from hypoxic damage by regulating the secretion and vasomotor function of VECs. The function of Danhong Injection was most remarkable.

6-Ketoprostaglandin F1 alpha ; metabolism ; Animals ; Apoptosis ; drug effects ; Blood Coagulation ; drug effects ; Cell Count ; Cells, Cultured ; Drugs, Chinese Herbal ; pharmacology ; Endothelial Cells ; drug effects ; metabolism ; Endothelins ; metabolism ; Factor VIII ; metabolism ; Fibrinolysis ; drug effects ; Fluorescent Antibody Technique ; Humans ; Infant, Newborn ; Injections ; Malondialdehyde ; metabolism ; Nitric Oxide ; metabolism ; Plasminogen Inactivators ; metabolism ; Rabbits ; Superoxide Dismutase ; metabolism ; Tissue Plasminogen Activator ; metabolism ; Umbilical Veins ; cytology

OBJECTIVETo evaluate the effect of sodium tanshinone IIA sulfonate (STS) in preventing postoperative peritoneal adhesions in rats and explore the mechanisms.

METHODSSixty SD rats were randomized into 4 equal groups, including a blank control group, adhesion model group, and high-, moderate-, and low-dose STS-treated groups, and were subjected to injuries of the parietal peritoneum and cecum to induce peritoneal adhesions, followed by intraperitoneal administration of saline and STS at the doses of 20, 10, and 5 mg/kg for 7 consecutive days, respectively. Another 15 untreated rats served as the blank control group. The adhesion scores in each group were recorded after the treatments; the activity of tissue-type plasminogen activator (tPA) in peritoneal lavage fluid was measured, tPA/PAI-1 protein ratio in the peritoneal tissue was determined by ELISA, and the expressions of TGF-β1 and collagen I were detected by immunohistochemistry. The anastomotic healing model was used to assess the impact of STS on wound healing.

RESULTSIntraperitoneal administration of STS effectively prevented peritoneal adhesion without affecting anastomotic healing in the rats. Compared with the adhesion model group, the STS-treated groups showed increased peritoneal lavage fluid tPA activity and tPA/PAI-1 ratio in the ischemic tissues with lowered TGF-β1 and collagen I expressions in the ischemic tissues.

CONCLUSIONSIntraperitoneal administration of STS can prevent peritoneal adhesion and enhance local fibrinolysis in rats, and these effects may be mediated by TGF-β signaling pathway.

Animals ; Cecum ; injuries ; pathology ; Collagen Type I ; metabolism ; Fibrinolysis ; Injections, Intraperitoneal ; Peritoneum ; injuries ; pathology ; Phenanthrenes ; pharmacology ; Plasminogen Activator Inhibitor 1 ; metabolism ; Postoperative Complications ; prevention & control ; Rats ; Rats, Sprague-Dawley ; Tissue Adhesions ; prevention & control ; Tissue Plasminogen Activator ; metabolism ; Transforming Growth Factor beta1 ; metabolism ; Wound Healing

OBJECTIVEThe exact mechanisms of defect closure in patients with perimembranous ventricular septal defect (PMVSD) remain unknown. We hypothesized that the expression of urokinase type plasminogen activator (uPA) and plasminogen activator inhibitor-1 (PAI-1) may mediate extracellular matrix (ECM) remodeling in aneurysms.

METHODSeven normal heart tricuspid septal leaflet and 33 aneurysms were collected in Shanghai Renji Hospital and Shanghai Children's Medical Center from January 2008 to June 2010. Immunohistochemical expression of uPA and PAI-1 in 4 normal heart valvular tissues and 15 aneurysms was detected with immunohistochemical methods. The expression of uPA and PAI-1 mRNA in 3 normal heart valvular tissues and 7 aneurysms was studied by real time fluorescent PCR; the protein expression of uPA and PAI-1 in 4 normal heart valvular tissues and 11 aneurysms was tested with Western blotting.

RESULTThe surface of the aneurysms were completely covered by endothelial cells. Two types of granulation tissue, myxoid and fibrous, were associated with the aneurismal formation. uPA were recognized predominantly in valvar interstitial cells (VICs) which located mainly in regions adjacent to the endothelium and smooth muscle cells of blood vessels. PAI-1 was found in both VICs which located mainly in granulation tissue and endothelial cells. Nine aneurysms expressed a higher uPA activity than 4 normal valvular tissues ((74.6±11.8)% vs. (49.5±7.4)%; t = 3.87, P = 0.003) and six aneurysms expressed a low uPA activity ((10.3±3.1)% vs. (49.5±7.4)%; t=11.78, P=0.000) and a high PAI-1 activity ((55.2±1.7)% vs. (50.8±3.8)%; t=2.55, P=0.034) using immunohistochemical methods. uPA / PAI-1 ratio of protein expression tested by Western blot was 0.88±0.22 in four normal heart vavular tissues; five aneurysms expressed high uPA activity and low PAI-1 activity and uPA/PAI-1 ratio was 4.26±2.04; while the other 6 cases expressed low uPA activity and high PAI-1 activity and uPA/PAI-1 ratio was 0.30±0.07; the difference among the three groups was statistically significant (P<0.05). The rate of uPA/PAI-1 in relative copy of mRNA expression among normal heart valvular tissue, high uPA expressed aneurysms and low uPA expressed aneurysms are also significantly different (2.14±0.17 vs. 0.45±0.04; 2.14±0.17 vs. 4.38±1.41, P<0.05) respectively.

CONCLUSIONThe expression of uPA and PAI-1 in VICs suggests that interactions among these molecules contribute to the aneurysm formation and development. This provides a potential mechanism for defect closure in patients with PMVSD.

Aneurysm ; pathology ; Blotting, Western ; China ; Endothelial Cells ; cytology ; Extracellular Matrix ; metabolism ; Granulation Tissue ; pathology ; Heart Septal Defects, Ventricular ; pathology ; Humans ; Immunohistochemistry ; Plasminogen Activator Inhibitor 1 ; metabolism ; RNA, Messenger ; Urokinase-Type Plasminogen Activator ; metabolism

OBJECTIVETo discuss the protective effects of Xin'ganbao Capsule (XC) on early kidney injury in streptozocin (STZ)-induced diabetic rats and its mechanisms.

METHODSTwenty-four male Wistar rats were selected to establish STZ induced diabetes mellitus (DM) model. After modeling they were randomly divided into the model group,the XC group (at the daily dose of 0.5 g/kg), and the benazepril group (at the daily dose of 4 mg/kg), 8 in each group. Another 8 rats were chosen as the blank control group. Rats in the model group and the blank control group were administered with equal volume of normal saline by gastrogavage for 8 successive weeks. The blood glucose was monitored by the end of the 4th week and the 8th week. The 24 h urine protein (24 hUP), blood urea nitrogen (BUN), and serum creatinine (SCr) were detected by the end of the 8th week. The transforming growth factor-beta1 (TGF-beta1), laminin (LN), collagen IV (Col-IV) expression were detected using immunohistochemical assay. The mRNA expressions of renal TGF-beta1, tissue inhibitor of matrix metalloproteinase-1 (TIMP-1), and plasminogen activator inhibitor-1 (PAI-1) were detected using RT-PCR. The pathological changes of the renal tissue were observed by HE, PAS, and Masson stain methods.

RESULTSCompared with the blank control group, hyperglycemia, polydipsia, polyphagia, polyuria, weight loss, emaciation, dry and dim body hair, and irritability appeared in the diabetic rats. After 8 weeks the symptoms of the two medication groups were attenuated. When compared with the blank control group, the 24 hUP, SCr, blood glucose, Col-IV, LN, TGF-beta1 positive expression ratio, the levels of TGF-beta1, TIMP-1, PAI-1 mRNA, the area of glomerular (GA), extracellular matrix (ECM), and ECM/GA all increased in the model group with statistical difference (P<0.01). The pathological changes showed obvious glomerular enlargement, the capillary loop expansion, the proliferation of the mesangial cells, increased mesangial matrix, widen and thicken glomerular basement membrane (GBM), and tubular derangement. The vacuolar degeneration and shedding could be seen in partial epithelial cells. The protein cast could also be seen with infiltration of interstitial inflammatory cells. Compared with the model group, each index of the two medication groups decreased with statistical difference (P<0.01). The pathological changes were less in the two medication groups. The mesangial cells were slightly proliferated and the mesangial matrix slightly increased. The mRNA expressions of SCr and PAI-1 were lower in the XC group than in the benazepril group (P<0.05). There was no statistical difference in the other indices between the two medication groups (P > 0.05). Conclusions XC had some protective effects and anti-glomerulosclerosis effects on early kidney injury in STZ-induced diabetic rats. Its mechanisms might be associated with down-regulating the mRNA expressions of TGF-beta1, TIMP-1, PAI-1, and Col-IV, reducing ECM and urine protein.

Animals ; Benzazepines ; therapeutic use ; Collagen Type IV ; metabolism ; Diabetes Mellitus, Experimental ; drug therapy ; metabolism ; pathology ; Drugs, Chinese Herbal ; pharmacology ; therapeutic use ; Extracellular Matrix ; metabolism ; Kidney ; pathology ; Laminin ; metabolism ; Male ; Plasminogen Activator Inhibitor 1 ; metabolism ; Rats ; Rats, Wistar ; Tissue Inhibitor of Metalloproteinase-1 ; metabolism ; Transforming Growth Factor beta1 ; metabolism

OBJECTIVEThe imbalance between extracellular matrix (ECM) synthesis and degradation induces the excessive ECM deposition and thus renal fibrosis. The decoction (A&A) which is a combination of two Chinese herbs, Astragalus membranaceus var. mongholicus and Angelica sinensis, has been shown to alleviate ECM production in animal models of chronic kidney diseases. In this paper, the effect of A&A on ECM degradation was investigated with interstitial fibrosis in rats.

METHODMale Wistar rats were randomly divided into sham, unilateral ureteral obstruction (UUO) and UAA (UUO plus A&A administration) groups. After administration of A&A (14 g x kg(-1) x d(-1)) by gavage for 3, 7 and 10 days, morphological changes were evaluated by HE, PAS and Sirius red staining technique. The expression of plasminogen activator inhibitor-1 (PAI-1) and tissue-type plasminogen activator (t-PA), the activity of PAI-1 and t-PA were determined by ELISA. The activity of matrix metalloproteinases (MMP-9, MMP-2), tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) were evaluated by gelatin zymography or reverse gelatin zymography, respectively.

RESULTMorphological analysis showed severe interstitial mononuclear cells infiltration, tubular atrophy, renal fibrosis and collagen expression in kidneys of UUO group, which was reduced by A&A administration (P < 0.05, UAA vs UUO group). Compared with the sham group, the expression of PAI-1 was significantly increased in UUO group by 63%, 91% and 112% at day 3, 7 and 10 respectively; and there were a remarkable decrease in UAA group by 44%, 43% and 52% at day 3, 7 and 10. The expression of active PAI-1 was strikingly increased in UUO group at day 3 [(30.5 +/- 23.8) ng x g(-1) vs. (0.0 +/- 0.0) ng x g(-1), P < 0.05)], day 7 [(36.5 +/- 11.2) ng x g(-1) vs. (0.0 +/- 0.0) ng x g(-1), P < 0.05)], and day 10 [(54.5 +/- 14.2) ng x g(-1) vs. (0.5 +/- 0.5) ng x g(-1), P < 0.05)]. The active PAI-1 was decreased in UAA group at day 7 [(14.9 +/- 0.5) ng x g(-1) vs. (36.5 +/- 11.2) ng x g(-1), P < 0.05] and day 10 [(15.4 +/- 4.8) ng x g(-1) vs. (54.5 +/- 14.2) ng x g(-1), P < 0.05]. The expression of t-PA was increased in UUO group only at day 3 [(58.1 +/- 16.5) microg x g(-1) vs. (30.1 +/- 17.3) microg x g(-1)], P < 0.05), meanwhile decreased in UAA group [(26.3 +/- 8.7) microg x g(-1) vs. (58.1 +/- 16.5) microg x g(-1), P < 0.05)]. But the expression of active t-PA was shown no significantly difference among the three groups. For MMP-2 and MMP-9 activity, they were significantly higher compared with the sham group in UUO group, but no significantly change after A&A treatment. The TIMP-1 activity was significantly increased in UUO group by 28% and 63% at day 7 and 10 respectively, significantly decreased in UAA group by 40% and 39% at the same time point.

CONCLUSIONThe anti-fibrosis effects of A&A might be associated with modulating the imbalance of PAs/PAIs system as well as MMPs/TIMPs system, thereby alleviate ECM accumulation and interstitial fibrosis.

Angelica sinensis ; chemistry ; Animals ; Astragalus Plant ; chemistry ; Drugs, Chinese Herbal ; administration & dosage ; Extracellular Matrix ; metabolism ; Fibrosis ; Humans ; Kidney ; enzymology ; metabolism ; pathology ; Kidney Diseases ; drug therapy ; enzymology ; metabolism ; pathology ; Male ; Matrix Metalloproteinase 1 ; metabolism ; Matrix Metalloproteinase 9 ; metabolism ; Plasminogen Activator Inhibitor 1 ; metabolism ; Rats ; Rats, Wistar ; Tissue Plasminogen Activator ; metabolism

OBJECTIVETo assess the influence of laparoscopic colorectal cancer resection on the peritoneal microstructure injury and expression of t-PA/PAI-1 molecules.

METHODSA total of 50 patients with colorectal cancer were prospectively enrolled between June 2011 and February 2012 in the Shanxi Provincial Hospital and were assigned into laparoscopic group (LO, n=27) and conventional laparotomy group (CO, n=23) based on patients expectancy and surgeon decision. Optical microscope and scanning electron microscope were employed for comparison of the postoperative peritoneal injury between LO and CO. Before and after surgery, t-PA and PAI-1 of peritoneal tissue were determined by ELISA in both groups.

RESULTSOptical microscope and scanning electronic microscopy scan indicated less serosal injury in LO group than that in CO group with regard to serosa integrity, continuity of covering adipocytes and mesothelial cells, and the aggregation level of inflammatory cells (P<0.01). The injury score was 38.22 in CO in and 14.67 in LO and the difference was statistically significant (P<0.01). No significant differences were found between LO and CO in terms of postoperative t-PA in the omentum, t-PA and PAI-1 in the intestinal serosa tissue (P>0.05), however PAI-1 in the omentum was significantly lower in LO group compared to CO group (P<0.05).

CONCLUSIONLaparoscopic radical resection for colorectal cancer causes less peritoneal structural injury and less influence on the fibrinolytic capacity, which may contribute to less postoperative adhesion.

Adolescent ; Adult ; Aged ; Colorectal Neoplasms ; metabolism ; surgery ; Colorectal Surgery ; adverse effects ; methods ; Female ; Humans ; Laparoscopy ; adverse effects ; Male ; Middle Aged ; Peritoneum ; metabolism ; pathology ; Plasminogen Activator Inhibitor 1 ; metabolism ; Prospective Studies ; Tissue Plasminogen Activator ; metabolism ; Young Adult

The balance between tissue-type plasminogen activator (t-PA) and plasminogen activator inhibitor type 1 (PAI-1) regulates fibrinolysis. PAI-1 expression increases in atherosclerotic arteries and vascular smooth muscle cells (VSMCs) are one of major constituents of atheroma. We investigated the impact of lysophosphatidylcholine (lysoPC), an active component of oxidized low-density lipoprotein, on the plasminogen activator system of the rat VSMCs. The lysoPC stimulated the protein and gene expressions of PAI-1 but did not affect the protein expression of t-PA. Fibrin overlay zymography revealed that lysoPC increased the activity of PAI-1 in the conditioned media, while concurrently decreasing that of free t-PA. Vitamin E inhibited the lysoPC-induced PAI-1 expression. Further, lysoPC increased the intracellular reactive oxygen species (ROS) formation. Caffeic acid phenethyl ester, an inhibitor of NF-kappaB, blocked this lysoPC effect. Indeed, lysoPC induced the NF-kappaB-mediated transcriptional activity as measured by luciferase reporter assay. In addition, genistein, an inhibitor of protein-tyrosine kinase (PTK), diminished the lysoPC effect, while 7,12-dimethylbenz[a]anthracene, a stimulator of PTK, stimulated PAI-1 production. In conclusion, lysoPC does not affect t-PA expression but induces PAI-1 expression in the VSMC by mediating NF-kappaB and the genistein-sensitive PTK signaling pathways via oxidative stress. Importantly, lysoPC stimulates the enzyme activity of PAI-1 and suppresses that of t-PA.
Animals ; Benz(a)Anthracenes/pharmacology ; Caffeic Acids/pharmacology ; Cells, Cultured ; Genistein/pharmacology ; Lipoproteins, LDL/metabolism ; Lysophosphatidylcholines/*pharmacology ; Muscle, Smooth, Vascular/cytology/*drug effects/metabolism ; NF-kappa B/antagonists & inhibitors/metabolism ; Oxidative Stress/drug effects ; Phenylethyl Alcohol/analogs & derivatives/pharmacology ; Plasminogen Activator Inhibitor 1/agonists/genetics/*metabolism ; Protein Kinase Inhibitors/pharmacology ; Protein-Tyrosine Kinases/antagonists & inhibitors/metabolism ; Rats ; Rats, Sprague-Dawley ; Reactive Oxygen Species/metabolism ; Signal Transduction/drug effects ; Tissue Plasminogen Activator/*metabolism ; Transcription, Genetic/drug effects ; Up-Regulation/drug effects ; Vitamin E/pharmacology

Toxoplasma gondii can modulate host cell gene expression; however, determining gene expression levels in intermediate hosts after T. gondii infection is not known much. We selected 5 genes (ALDH1A2, BEX2, CCL3, EGR2 and PLAU) and compared the mRNA expression levels in the spleen, liver, lung and small intestine of genetically different mice infected with T. gondii. ALDH1A2 mRNA expressions of both mouse strains were markedly increased at day 1-4 postinfection (PI) and then decreased, and its expressions in the spleen and lung were significantly higher in C57BL/6 mice than those of BALB/c mice. BEX2 and CCR3 mRNA expressions of both mouse strains were significantly increased from day 7 PI and peaked at day 15-30 PI (P<0.05), especially high in the spleen liver or small intestine of C57BL/6 mice. EGR2 and PLAU mRNA expressions of both mouse strains were significantly increased after infection, especially high in the spleen and liver. However, their expression patterns were varied depending on the tissue and mouse strain. Taken together, T. gondii-susceptible C57BL/6 mice expressed higher levels of these 5 genes than did T. gondii-resistant BALB/c mice, particularly in the spleen and liver. And ALDH1A2 and PLAU expressions were increased acutely, whereas BEX2, CCL3 and EGR2 expressions were increased lately. Thus, these demonstrate that host genetic factors exert a strong impact on the expression of these 5 genes and their expression patterns were varied depending on the gene or tissue.
Aldehyde Dehydrogenase/*genetics/metabolism ; Animals ; Brain/metabolism/parasitology ; Chemokine CCL3/*genetics/metabolism ; Early Growth Response Protein 2/*genetics/metabolism ; Gene Expression Profiling ; Humans ; Lung/metabolism/parasitology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Inbred Strains ; Nerve Tissue Proteins/*genetics/metabolism ; Organ Specificity ; Spleen/metabolism/virology ; Toxoplasma/*physiology ; Toxoplasmosis/*genetics/metabolism/parasitology ; Urokinase-Type Plasminogen Activator/*genetics/metabolism