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Yi-Xin Wang

Publications and source records attributed to Yi-Xin Wang.

13 recordsLinked to original sources

17 Beta-estradiol attenuates development of angiotensin II-induced aortic abdominal aneurysm in apolipoprotein E-deficient mice.

OBJECTIVE: Angiotensin II (Ang II) promotes vascular inflammation, accelerates atherosclerosis, and induces abdominal aortic aneurysm (AAA). These changes were associated with activation of nuclear factor (NF)-kappaB-mediated induction of proinflammatory genes. The incidence of AAA in this model was higher in male than in female mice, and the vascular effects of estrogen may be associated with anti-inflammatory actions. The present study was undertaken to test the hypothesis that estrogen can attenuate Ang II-induced AAA in apolipoprotein E-deficient mice via its anti-inflammatory mechanism. METHODS AND RESULTS: Infusion of Ang II (1.44 mg/kg per d for 1 month) induced AAA in 90% of the animals (n=20) with an expansion of the suprarenal aorta (diameter 1.9+/-0.14 mm versus <1 mm in normal mice). In mice treated with 17beta-estradiol (E2, 0.25-mg subcutaneous pellets), Ang II induced AAA only in 42% of the animals (n=19) with a significant reduction of average diameters of the suprarenal aorta (1.5+/-0.14 mm). E2 also decreased the expressions of intracellular adhesion molecule-1, vascular cellular adhesion molecule-1, E-selectin, monocyte chemotactic protein-1, and macrophage-colony stimulating factor in the aorta. CONCLUSIONS: These data suggest that attenuation of AAA by E2 is associated with inhibition of proinflammatory gene expression.

Angiotensin II↗

Urokinase-type plasminogen activator plays a critical role in angiotensin II-induced abdominal aortic aneurysm.

We have previously demonstrated that urokinase-type plasminogen activator (uPA) is highly expressed in the aneurysmal segment of the abdominal aorta (AAA) in apolipoprotein E-deficient (apoE-/-) mice treated with angiotensin II (Ang II). In the present study, we tested the hypothesis that uPA is essential for AAA formation in this model. An osmotic minipump containing Ang II (1.44 mg/kg per day) was implanted subcutaneously into 7- to 11-month-old male mice for 1 month. Ang II induced AAA in 9 (90%) of 10 hyperlipidemic mice deficient in apoE (apoE-/-/uPA+/+ mice) but in only 2 (22%) of 9 mice deficient in both apoE and uPA (apoE-/-/uPA-/- mice) (P<0.05). Although the expansion of the suprarenal aorta was significantly less in apoE-/-/uPA-/- mice than in apoE-/-/uPA+/+ mice, the aortic diameters of the aorta immediately above or below the suprarenal aorta were similar between the 2 groups. Ang II induced AAA in 7 (39%) of 18 strain-matched wild-type C57 black/6J control mice. The incidence was significantly higher in atherosclerotic apoE-deficient (apoE-/-) mice, in which 8 (100%) of 8 mice developed AAA. Only 1 (4%) of 27 uPA-/- mice developed AAA after Ang II treatment. We conclude the following: (1) uPA plays an essential role in Ang II-induced AAA in mice with or without preexisting hyperlipidemia and atherosclerosis; (2) uPA deficiency does not affect the diameter of the nonaneurysmal portion of the aorta; and (3) atherosclerosis and/or hyperlipidemia promotes but is not essential for Ang II-induced AAA formation in this model.

Angiotensin II↗

Activated thrombin-activatable fibrinolysis inhibitor attenuates spontaneous fibrinolysis of batroxobin-induced fibrin deposition in rat lungs.

Studies have shown that inhibition of TAFI by small peptides enhances pharmacological effects of tPA in animal models of thrombosis, suggesting that TAFI modulates the fibrinolytic system. In this study, we investigated the effect of activated human TAFI (TAFIa) on endogenous fibrinolysis in a rat model of intravascular fibrin deposition. (125)I-labeled fibrinogen was injected intravenously followed by a bolus injection of batroxobin, a thrombin-like enzyme. Batroxobin cleaved fibrinogen to form insoluble fibrin that was deposited in tissues, including the lungs. This was shown by a decrease of radioactivity in the blood as a result of consumption of (125)I-labeled fibrinogen and an elevation of radioactivity in the lungs 5 min following batrox-obin administration. Endogenous fibrinolysis was detected by a gradual increase in radioactivity in the blood and a decrease in radioactivity in the lungs at 30 min, an indication of radiolabeled fibrin degradation products (FDPs) being released into the circulation from the tissues. Intravenous administration of human TAFIa dose-dependently attenuated the later phase reduction of radioactivity in the lungs. When the dose of TAFIa was 218 micro g/kg, giving a peak plasma level of TAFIa 0.9 +/- 0.05 micro g/ml, the spontaneous fibrinolysis was completely prevented. These results provide direct evidence that an increase in circulating TAFIa impairs endogenous clot lysis in a rat model of fibrin deposition.

Animals↗

Modulation of vascular inflammation by PPARs.

The activation of cells in atherosclerotic lesions leads to the release of proinflammatory molecules and the onset of a chronic inflammatory response. Recent evidence suggests that peroxisome proliferator-activated receptors (PPARs) exert their antiinflammatory activities in vascular and immunological cell types such as endothelial cells, vascular smooth muscle cells and monocytes/macrophages. In these cells, PPARs regulate the gene expression of key proteins involved in the vascular inflammation contributing to atherogenesis. By modulating transcription of proinflammatory genes such as cytokines, chemokines, endothelial cell adhesion molecules and metalloproteinases, one can affect the events involved in atherogenesis, such as monocyte/macrophage and lymphocyte recruitment to the arterial wall and foam cell formation. Thus, PPAR agonists have emerged as a potential tool to modulate the inception and progression of atherosclerosis by exerting direct antiinflammatory and antiatherogenic actions at the level of the arterial wall. In this review, we will describe the current understanding of PPARs, the antiinflammatory activities of PPAR agonists and their proposed mechanisms of action.

Angiotensin II↗

Cryopreservation-induced decrease in heat-shock protein 90 in human spermatozoa and its mechanism.

AIM: To study the protein changes of spermatozoa associated with sperm motility during sperm cryopreservation and its mechanism. METHODS: In 18 healthy men, the seminal sperm motility and HSP90 levels were studied before and after cryopreservation using SDS-PAGE, Western blotting and computerized image analysis. RESULTS: The sperm motility declined significantly after cryopreservation (P<0.01). The average grey level and the integrated grey level of sperm HSP90 before cooling were 34.1+/-3.2 and 243.0+/-21.6, respectively, while those after thawing were 23.2+/-2.5 and 105.7+/-28.5, respectively. Both parameters were decreased significantly (P<0.01). No HSP90 was found in the seminal plasma before and after cryopreservation. CONCLUSION: HSP90 in human spermatozoa was decreased substantially after cryopreservation. This may result from protein degradation, rather than leakage into the seminal plasma.

Blotting, Western↗

[Progression of semen cryopreservation and its relationship with assisted reproductive technology].

The aim of semen cryopreservation research is to elevate the proportion of competent spermatozoa after thawing. By means of molecular biology, the research of spermatozoa injury during cryopreservation reaches molecular level. In each stage of cryopreservation, there exists its own optimal condition for cooling. Cryopreservation medium still need to be improved. Men should pay more attention to the field of spermatozoa function. Assisted reproductive technology (ART) has a close relationship with the technology of semen cryopreservation. The latter's development will improve the former.

Animals↗

[Experimental research on human spermatozoa membrane proteins by two-dimensional gel electrophoresis].

OBJECTIVES: To analyze human spermatozoa membrane proteins by two-dimensional gel electrophoresis and to provide a basis for drawing the protein map of normal human spermatozoa membrane proteins. METHODS: Spermatozoa were purified by Percoll density centrifugation, and spermatozoa membrane proteins were analyzed by two-dimensional gel electrophoresis using isoelectric focusing and polyacrylamide gel electrophoresis. RESULTS: About 800 protein spots could be identified by the imaging analysis system. The molecular weight and isoelectric point of most proteins were 20,000 to 100,000 and 3.0 to 7.0 respectively. CONCLUSIONS: There are more than 800 types of proteins in the human spermatozoa membrane. The spermatozoa membrane protein can be identified with a certain precision by two-dimensional gel electrophoresis.

Electrophoresis, Gel, Two-Dimensional↗

[Seminal plasma angiotensin II detection and its clinical implication].

OBJECTIVE: To investigate the variation of seminal plasma angiotension II (Ang II) in infertile men and its clinical implication. METHODS: Ang II values in paired blood plasma and seminal plasma from 43 infertile men(13 azoospermia, 8 asthenozoopermia, 17 asthenozoospermia and 5 cases with normal semen parameters) and 10 normal controls were obtained by SPE-HPLC-RIA. All semen samples with spermatozoa were analyzed by CASA for sperm count, motility and other parameters. Acrosome reaction rate (AR) was assessed by triple-stain. RESULTS: The mean concentration of seminal plasma Ang II was 4 times as high as that of blood plasma in all patients and controls (P < 0.01), but there was no correlation between them. The seminal plasma Ang II of azoospermic patients was higher than that of other infertile men and controls(P < 0.05), but no difference was found between the latter two groups. There was no correlation between seminal plasma Ang II values and other traditional parameters of sperm together with AR. CONCLUSIONS: Seminal plasma Ang II may be secreted locally in male reproductive tract. In addition to testis and epididymis, prostate and/or seminal vesicle may also be the source of it. The reason why seminal plasma Ang II of azoospermic patients is higher than that of others remains unknown. Further study is required to clarify the exact role of seminal plasma Ang II in the mechanisms of male fertility regulation.

Acrosome↗

Angiotensin II injures the arterial wall causing increased aortic stiffening in apolipoprotein E-deficient mice.

Cardiovascular diseases, such as atherosclerosis and hypertension, are associated with arterial stiffening. Previous studies showed that ANG II exacerbated atherosclerosis and induced hypertension and aneurysm formation in apolipoprotein E-deficient (apoE-KO) mice. The aim of the present study was to examine the effects of chronic treatment of ANG II on the arterial elastic properties in apoE-KO mice. We hypothesized that ANG II will injure the arterial wall resulting in increased arterial stiffening. Male apoE-KO mice were infused with either ANG II (1.44 mg. kg(-1). day(-1)) or vehicle (PBS) for 30 days. ANG II treatment accelerated atherosclerosis in the carotid artery by sixfold (P < 0.001) and increased blood pressure by 30% (P < 0.05). Additionally, our data demonstrated that ANG II increased arterial stiffening using both in vivo and in vitro methods. ANG II significantly increased pulse wave velocity by 36% (P < 0.01) and decreased arterial elasticity as demonstrated by a more than 900% increase in maximal stiffening (high strain Young's modulus) compared with vehicle (P < 0.05). These functional changes were correlated with morphological and biochemical changes as demonstrated by an increase in collagen content (60%), a decrease in elastin content (74%), and breaks in the internal elastic lamina in the aortic wall. In addition, endothelium-independent vasorelaxation to sodium nitroprusside was impaired in the aortic rings of ANG II-treated mice compared with vehicle. Thus, the present data indicate that ANG II injures the artery wall in multiple ways and arterial stiffening may be a common outcome of ANG II-induced arterial damage.

Acetylcholine↗

Reduction of cardiac functional reserve and elevation of aortic stiffness in hyperlipidemic Yucatan minipigs with systemic and coronary atherosclerosis.

To test the hypothesis that cardiac functional reserve is reduced in animals with severe atherosclerosis, Yucatan minipigs were fed a high-cholesterol diet (Chol) for 8 months. Half of them was made diabetic, an additional risk factor for atherosclerosis, with streptozotocin (STZ). Another group of age-matched minipigs were fed a normal diet as controls. At the end of the treatment period, animals were instrumented for the measurement of cardiovascular hemodynamic parameters under isoflurane anesthesia. Cardiac functional reserve was measured by the magnitude of the inotropic response to isoproterenol stress. Hyperlipidemic minipigs developed severe atherosclerotic plaques in the aorta, coronary and iliac artery, accompanied by an increase in the aortic stiffness indexed by increases in pulse wave velocity and augmentation index. These vascular changes were more severe in STZ-induced insulin-dependent diabetes mellitus. The isoproterenol-induced increase in left ventricular contractility (dP/dt) and relaxation (-dP/dt) and, consequently, cardiac output were also significantly reduced in both the Chol groups with or without STZ, compared to control group. Thus, cardiac functional reserve measured by isoproterenol-stimulated responses was reduced in atherosclerotic minipigs, which was further diminished in diabetes.

Animals↗

[The effects of testosterone undecanoate on relaxation of rat corpus cavernosum smooth muscle in vitro].

OBJECTIVES: To investigate the role of Undecanoate (Andriol), as a kind of testosterone, in regulating the relaxation of isolated rat corpus cavernosum in vitro. METHODS: The castrated rats were given high and low dosage Andriol respectively, compared with intact and castrated rats. After treatment of 4 weeks, the corpora cavernosa were cut, trimmed as to strips. Norepinephrine(NE) was added to contract each of the tissue strips. Next, sodium nitroprusside(SNP), electric functional stimulation(EFS) were used to relax the strips. Percent relaxations were examined. RESULTS: High-dose Andriol(20 mg/kg) was significantly effective to castrated rats on percent relaxation induced by 10(-3) mol/L SNP and EFS. Low-dose Andriol(10 mg/kg) was also effective to relax strips induced by 10(-3) mol/L SNP. According to statistics, the differences were significant (P < 0.01). CONCLUSIONS: The percent relaxations of castrated rats were increased after taking Andriol, and it could increase the relaxation of corpara cavernosa.

Animals↗

[Correlation of the factors on benign prostatic hyperplasia combined with obstruction].

Benign prostate obstruction(BPO) means bladder outlet obstruction (BOO) due to benign prostatic hyperplasia (BPH), which concerns BPH, and lower urinary tract symptoms(LUTS). To treat the BPO is the main purpose of therapy on BPH in clinic. This review includes recent advances in study of changes on urodynamics(UDS), morphology, prostatic composition, which occur in BPO.

Humans↗

[Effect of aging on male sexual function in 93 patients using international index of erectile function].

OBJECTIVES: To investigate the influence of aging on male sexual function. METHODS: The study selected 93 ED patients, aged from 23 to 64, who responded to the International Index of Erectile Function (IIEF) questionnaire. The questionnaire includes 15 items related to male sexual activity, which are organized into 5 domains, namely, erectile function (EF), orgasmic function (OF), sexual desire (SD), intercourse satisfaction (IS) and overall satisfaction (OS). For statistical analysis, ANOVA with DUNCAN test was conducted, and statistical significance was set at P < 0.05. Some other risk factors of ED such as hypertension, diabetes etc. had been excluded. RESULTS: According to the age, the subjects were divided into 5 groups. With age increasing, the proportion of moderate and severe in each group increased from 16.17% to 57.14%, whereas EF score decreased from (19.50 +/- 4.64) to (15.27 +/- 5.64), OF score decreased from (6.93 +/- 2.86) to (5.62 +/- 2.94), SD score decreased from (6.33 +/- 1.63) to (4.50 +/- 2.94), IS score decreased from (10.17 +/- 1.94) to (6.93 +/- 2.90), OS score decreased from (5.00 +/- 0.89) to (3.15 +/- 1.84). The tendency took on linearity (P < 0.01). Aging was negatively correlated to above mentioned scores (r = 0.98, P < 0.01). CONCLUSION: Aging could be thought as a risk factor of ED, which is negatively correlated with male's EF, OF, IS, OS and SD scores, furthermore. IIEF questionnaire is a useful tool assessing epidemiology of ED.

Adult↗