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Biomedical subjects

Prasong Siriviriyakul

Publications and source records attributed to Prasong Siriviriyakul.

11 recordsLinked to original sources
PubMed2006

The vascular effect of genistein: what is its mechanism, nitric oxide or PGI2?

To determine the effects and mechanism(s) of genistein on endothelial functions, the model of mesenteric-chamber with intravital fluorescence videomicroscopy and image analysis were used. After preconstriction with norepinephrine (NE; 10(-6) M), vascular responses to different doses of genistein (10(-2)-10(-7) M) were recorded with real time video-camera. The mechanism(s) of vasodilation was also determined by using N(omega)-L-arginine methyl ester (L-NAME; 100 microM), the inhibitor of nitric oxide synthase (NOS inhibitor), and/or indomethacin (INDO; 10 microM), cyclooxygenase inhibitor. The results indicated that the topical application of 10(-2)-10(-7) M genistein on mesenteric microvessels caused the increase in arteriolar diameters from 33% to 48%, respectively. The effects of genistein on mesenteric endothelial-dependent vasodilatation could be mediated through both L-arginine/NO and cyclooxygenase pathways. Our finding indicated that genistein could induce endothelial-dependent vasodilation similar to 17beta-estradiol.

Animals↗
PubMed2006

Microvascular disease and endothelial dysfunction in chronic kidney diseases: therapeutic implication.

This paper was aimed to study biomarkers of endothelial injury in chronic kidney diseases. Fifty chronic kidney disease patients were subject to the following determinations: (i) circulating endothelial cells, (ii) soluble VCAM-1, (iii) transforming growth factor beta (TGFB), and (iv) intrarenal hemodynamics. Increased number of circulating endothelial cells was significantly observed. A significant depletion of vascular endothelial growth factor (VEGF) or a depleted VEGF/TGFB ratio was also documented. Results showed that sVCAM was not significantly different from normal control. Intrarenal hemodynamic alteration demonstrated a characteristic of hemodynamic maladjustment. Since increased number of circulating endothelial cells is a sensitive biomarker for endothelial cell injury in chronic kidney diseases, such injury is supported by the depletion of VEGF. The endothelial cell loss correlates with the glomerular endothelial dysfunction characterized by hemodynamic maladjustment at the efferent arteriole and reduction in peritubular capillary flow. In conclusion, correction of such hemodynamic maladjustment with multidrug vasodilators can effectively restore renal function in chronic kidney diseases.

Biomarkers↗
PubMed2006

Genistein replacement therapy on endothelial dysfunction and bone loss in bilateral ovariectomized rats.

The objective of this study is to examine roles of genistein in postmenopausal induced-endothelial dysfunction and bone loss, the ovariectomized (OVX) rat model was used. The animals were divided into three groups of sham treated with vehicle (DMSO 100 microl/day; Sham(veh)), OVX treated with vehicle (OVX(veh)) and OVX treated with genistein (0.25 mg/kg/day; OVX(gen)). At 3 and 7 weeks after the surgery, endothelial dysfunction in mesenteric microcirculation of each group was determined by using intravital fluorescence microscopy and analyzed with digital image software. The parameters of bone mass density (BMD) and bone formation marker were represented by percentage of ash/dry matter and osteocalcin activity (using radioimmunoassay (RIA)), respectively. Mean arterial pressures (MAP) in OVX(veh) groups were significantly increased compared to their aged-matched sham groups (p<0.05). Interestingly, the treatment of genistein could significantly attenuate this abnormality (p<0.001). Besides, it could increase the vascular response to acetylcholine (Ach; 10(-6) M) significantly compared to OVX-rats (p<0.05). Moreover, BMD and osteocalcin activity were significantly increased in Ovx(gen) as well. Therefore, our findings suggested that genistein supplementation could effectively prevent endothelial dysfunction and bone loss in OVX-rat model.

Animals↗
PubMed2004

Hemodynamic maladjustment and disease progression in nephrosis with FSGS.

Idiopathic nephrotic syndrome (NS) associated with focal segmental glomerulosclerosis (FSGS) and severe renal function impairment is usually refractory to the conventional treatment and progresses to end-stage renal disease. Herein, we reported 10 patients with NS-FSGS who had initially had CCr 34 +/- 12 mL/min/1.73 m2 (normal 120 mL/min/1.73 m2), FE Mg 7.8 +/- 2.6% (normal 2.2%), 24-h urinary protein 3.1 g (normal <200 mg) and been followed up for over 10 years. The initial intrarenal hemodynamic study revealed a marked elevation of efferent arteriolar resistance (RE 17289 +/- 8636 dyne x s x cm(-5); normal 3000 dyne x s x cm(-5)), intraglomerular hypertension (PG 57 +/- 1 mm Hg; normal 52 mm Hg), hyperfiltration (FF 0.24; normal 0.2), marked reductions in GFR 35 +/- 17 mL/min/1.73 m2, renal plasma flow (RPF 159 +/- 61 mL/min/1.73 m2; normal 600 mL/min/1.73 m2) and peritubular capillary flow (PTCF 123 +/- 57 mL/min/1.73 m2; normal 480 mL/min/1.73 m2). Such a hemodynamic alteration indicated a hemodynamic maladjustment with a preferential constriction at RE. Treatment consists of multidrugs, namely angiotensin converting enzyme inhibitor, calcium channel blocker, antiplatelet and anticoagulant, with or without angiotensin II receptor antagonist. Following the treatment, correction of hemodynamic maladjustment has been achieved which is characterized by reductions in RE 6046 +/- 2191 dyne x s x cm(-5), PG 52 +/- mm Hg, FF 0.19 +/- 0.1 and increments in RPF 341 +/- 118 mL/min/1.73 m2, PTCF 280 +/- 106 mL/min/1.73 m2 and GFR 64 +/- 17 mL/min/1.73 m2. Coinciding with hemodynamic improvement, there has been a steadily increased creatinine clearance and improvement in FE Mg 4.3 +/- 2.6% and suppression of proteinuria 0.29 +/- 0.4 g/24 h after the period of follow-up of greater than 10 years.

Disease Progression↗
PubMed2004

Glomerular endothelial dysfunction in chronic kidney disease.

A dysfunctioning glomerular endothelium was demonstrated in chronic kidney disease (CKD) patients by means of in vitro endothelial cell cytotoxicity test and of in vivo intrarenal hemodynamic study. An enhanced endothelial cell cytotoxicity in CKD patients was 26.5 +/- 12% as compared to 0.4 +/- 1% of control. An altered intrarenal hemodynamics revealed 1) a reduction in renal plasma flow, 190 +/- 67 mL/min/1.73 m2 versus control 595 +/- 45 mL/min/1.73 m2, and in peritubular capillary flow, 149 +/- 55 mL/min/1.73 m2 versus control 479 +/- 46 mL/min/1.73 m2, 2) an elevated intraglomerular hydrostatic pressure, 55 +/- 2 mmHg versus control 51 mmHg, elevated afferent arteriolar resistance, 13184 dyne x s x cm(-5) versus control 2443 +/- 154 dyne x s x cm(5), and elevated efferent arteriolar resistance, 13591 +/- 7591 dyne x s x cm(-5) versus control 3062 +/- 177 dyne x s x cm(-5). Both enhanced endothelial cell cytotoxicity and altered intrarenal hemodynamics reflect glomerular endothelial dysfunction which is likely responsible for the renal disease progression in CKD.

Case-Control Studies↗
PubMed2004

Correction of peritubular capillary flow reduction with vasodilators restores function in focal segmental glomerulosclerotic nephrosis.

Due to the previously therapeutic failure in treating eleven focal segmental glomerulosis (FSGS) nephrotic patients (group I) with prednisolone, cyclophosphamide and antihypertensive agents (reserpine, hydralazine or prazosin) who all entered end-stage renal disease, we prospectively evaluate 18 FSGS nephrotic patients who have been treated with combined formula consisting of ACEI, AIIRA, CCB, antiplatelet+/-heparin; group II. All the patients were subject to renal function studies namely creatinine clearance, fractional excretion of magnesium (FE Mg) and intrarenal hemodynamics. Treatment outcome of patients in group II was comparatively assessed before and after therapy. Clinical profiles were comparatively matched between groups I and II. The intrarenal hemodynamic study in all nephrotic patients revealed hemodynamic maladjustment characterized by preferential constriction at the efferent arteriole. Such constriction induced intraglomerular hypertension and exaggeratedly reduced peritubular capillary flow (PTCF). Following treatment with combined formula (group II), reductions in efferent arteriolar resistance and intraglomerular hydrostatic pressure were observed in conjunction with the increases in PTCF and glomerular filtration rate in all 18 patients. Correction of hemodynamic maladjustment with combined formula effectively restores renal function and thereby prevents the renal disease progression in FSGS nephrosis.

Adolescent↗
PubMed2004

Ganoderma lucidum suppresses endothelial cell cytotoxicity and proteinuria in persistent proteinuric focal segmental glomerulosclerosis (FSGS) nephrosis.

A persistent proteinuria is commonly observed in nephrotic patient with focal segmental glomerulosclerosis (FSGS) under treatment with prednisolone+/-cyclophosphamide or with vasodilators (ACEI+AII receptor antagonist, calcium channel blocker and antiplatelet agent). Fourteen such patients with persistent proteinuria were subject to be treated with Ganoderma lucidum. Initial study revealed an enhanced endothelial cell cytotoxicity induced by patient's serum, and an altered immunocirculatory balance with predominant proinflammatory cytokine TNF alpha activity in the presence of defective anti-inflammatory cytokine interleukin-10. Treatment with Ganoderma lucidum suppressed endothelial cell cytotoxicity, restored immunocirculatory balance and successfully suppressed proteinuria in all of these 14 patients.

Anti-Inflammatory Agents↗
PubMed2003

A hemodynamically mediated mechanism of renal disease progression in severe glomerulonephritides or nephrosis.

Glomerular endothelial cell (GEC) dysfunction due to oxidative stress and enhanced proinflammatory cytokines plays an important role in inducing proteinuria and procoagulant activity, namely blood hypercoagulability, hyperviscosity and local intravascular coagulation and altered hemorheology in NS. A dysfunctioning GEC releases fewer endothelium-dependent vasodilators but produces more vasoconstrictors. Severe intrarenal hemodynamic alteration associated with hemodynamic maladjustment with preferential constriction at the efferent arteriole has been uniquely implicated in severe GN and NS-FSGS. Such a constriction exerts three significant hemodynamic impacts. Proximal to the efferent arteriolar constriction, it induces (i) an overestimated GFR due to hyperfiltration and (ii) an elevated intraglomerular hydrostatic pressure. Distal to the efferent arteriolar constriction, it (iii) exaggeratedly reduces PTCF which correlates with the TIF.

Disease Progression↗
PubMed2003

Treatment of glomerular endothelial dysfunction in steroid-resistant nephrosis with Ganoderma lucidum, vitamins C, E and vasodilators.

Glomerular endothelial dysfunction is believed to be responsible for the proteinuria and nephronal damage, namely tubulointerstitial fibrosis and glomerulosclerosis, observed in severe nephrosis such as focal segmental glomerulosclerosis. A dysfunctioning glomerular endothelium is likely to be induced by oxidative stress and oxidized LDL as well as altered immunocirculatory balance with a defective anti-inflammatory pathway. A defective release of vasodilator inconjunction with enhanced production of angiotensin II induces hemodynamic maladjustment by preferential constriction at the efferent arteriole. Such a hemodynamic maladjustment exerts two significant hemodynamic impacts. Close to the efferent constriction, it induces intraglomerular hypertension and glomerulosclerosis. Far from the efferent constriction, it reduces peritubular capillary flow, which eventually leads to tubulointerstitial fibrosis. Treatment with a vasodilator improves the hemodynamic maladjustment but does not completely suppress proteinuria. A successful suppression of proteinuria is accomplished by using Ganoderma lucidum and vitamins C and E. The beneficial effect of Ganoderma lucidum appears to be multifactorial, including the modulation of immunocirculatory balance, antilipid, vasodilator, antiplatelet and improved hemorheology. Together with vitamins C and E, this helps to neutralize oxidative stress and suppress the toxic effect to the glomerular endothelial function.

Adrenal Cortex Hormones↗
PubMed2003

Glomerular endothelial cytotoxicity and dysfunction in nephrosis with focal segmental glomerulosclerosis.

Glomerular endothelial cell dysfunction (GED) with defective release of vasodilator has been delineated in nephrosis (NS) in vivo and in vitro studies. In NS with focal segmental glomerulosclerosis (FSGS), an immunocirculatory balance may be impaired due to defective anti-inflammatory cytokine. This study aimed at simultaneous determination of both proinflammatory cytokine (tumor necrosis factor alpha) and an anti-inflammatory cytokine (interleukin-10) in NS with FSGS. An endothelial cell cytotoxicity (ECC) was also examined using nephrotic serum. It was shown that (1) the initial endothelial cell cytotoxicity was significantly different from the control, (2) ratio between tumor necrosis alpha and interleukin-10 was significantly elevated, and (3) intrarenal hemodynamics was changed significantly.

Endothelium, Vascular↗