Changes of serum soluble P-selectin and tumor necrotic factor-alpha in patients with CMV induced acute coronary syndrome / 中华实验和临床病毒学杂志

<p><b>OBJECTIVE</b>To explore the changes and relationship between serum soluble P-selectin, tumor necrosis factor-alpha (TNF-alpha) in coronary heart disease patients with acute coronary syndrome (ACS) and human cytomegalovirus (HCMV) infection.</p><p><b>METHODS</b>The levels of circulating soluble P-selectin, TNF-alpha, HCMV-IgM and HCMV-IgG were determined by enzyme-linked immunosorbent assay (ELISA) in 79 cases for ACS group, 30 cases for stable angina (SA) group and 30 healthy control cases.</p><p><b>RESULTS</b>(1) The serum positive rate of HCMV-IgM and HCMV-IgG in the ACS, SA and healthy control groups were 30.4% (24/79), 10.0% (3/30) and 6.7% (2/30); 86.1% (68/79), 80.0% (24/30) and 53.3% (16/30), respectively. Positive rate of HCMV-IgM in the ACS was higher than those in SA and healthy control groups (P < 0.01), positive rate of HCMV-IgG in the ACS and SA groups were higher than that of the healthy control group (P < 0.01). (2) Compared with the SA group and healthy control group, the levels of the serum soluble P-selectin and TNF-alpha were significantly higher in patients with ACS [(6437.3 +/- 666.9) pg/ml vs. (1520.0 +/- 112.7) pg/ml and (1481.0 +/- 109.1) pg/ml, (56.2 +/- 18.4) pg/ml vs. (27.3 +/- 13.7) pg/ml and (28.1 +/- 11.3) pg/ml], respectively, P < 0.01). The AMI group, compared with the UA group in the ACS group, had significantly higher levels of the serum soluble P-selectin and TNF-alpha (P < 0.01). Compared with the SA group, the levels of the serum soluble P-selectin and TNF-alpha were not significantly different in healthy control group. (3) The levels of the serum soluble P-selectin and TNF-alpha in HCMV-IgM positive patients were significantly higher than the HCMV-IgM negative patients in the ACS group (P < 0.01).</p><p><b>CONCLUSION</b>The chronic infection with HCMV might injure endothelial cells that subsequently contribute to the formation and progression of atherosclerosis, the acute infection with HCMV may induce increased serum levels of soluble P-selectin and TNF-alpha that might participate in acute coronary events.</p>

Vasonatrin peptide attenuates the enhancement of electrically-induced intracellular calcium transient by isoproterenol in rat cardiac myocytes / 生理学报

The purpose of this study was to investigate the effects of vasonatrin peptide (VNP) on electrically-induced intracellular calcium ([Ca(2+)](i)) transient and mechanism of the effects in the cardiac myocytes. The [Ca(2+)](i) transient was measured with a fluoremetric method. The effects of HS-142-1, 8-Br-cGMP and methylene blue (MB) on [Ca(2+)](i) transient in cardiac myocytes were also determined. Isoproterenol (Iso) at 10(-10)~10(-6) mol/L augmented electrically-induced [Ca(2+)](i) transient dose-dependently, which was (13+/-8)% (P>0.05), (26+/-13)% (P< 0.05), (66+/-10)% (P<0.01), (150+/-10)% (P<0.01) and (300+/-25)% (P<0.01), respectively. These effects were blocked by an beta-adrenergic bloker propranolol (10(-6) mol/L). The effect of Iso (10(-8) mol/L) on [Ca(2+)](i) transient was attenuated in a dose-dependent manner by VNP at 10(-10)~10(-6) mol/L, which was (99+/-3)% (P>0.05), (96+/-2)% (P<0.05), (84+/-6)% (P<0.01), (66+/-3)% (P<0.01) and (62+/-3)% (P<0.01), respectively. 8-Br-cGMP (10(-7)~10(-3) mol/L) aslo attenuated 10(-8) mol/L Iso-induced [Ca(2+)](i) transient dose-dependent. The effect of VNP on [Ca(2+)](i) transient was almost abolished in the presence of HS-142-1 (2x10(-5) mol/L), an antagonist of the natriuretic peptide guanylate cyclase (GC) receptors. MB (10(-5) mol/L), an inhibitor of GC, not only blocked the effect of VNP in myocytes, but also augmented electrically-induced [Ca(2+)](i) transient. VNP and HS-142-1 themselves did not change the [Ca(2+)](i) transient in the cardiac myocytes significantly. But MB augmented the [Ca(2+)](i) transient in the cardiac myocytes significantly. These results suggest that VNP attenuates [Ca(2+)](i) transient induced by Iso. This effect is possibly achieved by binding VNP with the natriuretic peptide GC receptors in the myocytes, leading to an increase in intracellular cGMP.

Preparation of hollow fiber bioreactor for culturing pig hepatocytes / 中华肝脏病杂志

<p><b>OBJECTIVE</b>To study the method of preparing the hollow fiber bioreactor for culturing pig hepatocytes.</p><p><b>METHODS</b>Hepatocytes were isolated from experimental suckling minipigs by two-step perfusion with collagenase, and seeded onto hollow fiber bioreactor, then cultured with an artificial capillary cell culture system. The albumin-excretion, lidocaine-transforming rate, lactate dehydrogenase (LDH) release and the cell viability in bioreactors were examined.</p><p><b>RESULTS</b>The porcine albumin could be detected by SDS/PAGE on the 2nd, 4th, 6th day. The rates of lidocaine-transforming ranged from 89.6% to 96.1%. The release of LDH into the culture medium increased from (23.7+/-4.6) U/L to (127.8+/-17.4) U/L (F=39.582, P<0.01) during the experiments, and the viability of pig hepatocytes in hollow fiber bioreactor reduced from 95.8%+/-0.3% to 83.8%+/-4.7% (t=5.135, P<0.01).</p><p><b>CONCLUSION</b>The hollow fiber bioreactor for culturing pig hepatocytes can be prepared by artificial capillary cell culture system, which provides a certain liver-specific function in 1 week.</p>

Vasorelaxing role of vasonatrin peptide in human intramammary artery in vitro / 生理学报

The purpose of this study was to investigate the vasorelaxing effect of vasonatrin peptide (VNP) on human intramammary artery (HIMA).The vasorelaxing effect of VNP on HIMA was measured by means of perfusion in vitro. The effects of HS-142-1, TEA, 8-Br-cGMP and methylene blue (MB) were also observed. It was found that VNP caused a concentration-dependent relaxation in HIMA which was independent of the endothelium. 8-Br-cGMP (0.1-1000 micromol/L) also caused a concentration-dependent relaxation in HIMA. The vasorelaxing effect of VNP disappeared in the presence of HS-142-1 (20 micromol/L), an antagonist of the natriuretic peptide guanylate cyclase (GC) receptor. MB (10 micromol/L), an inhibitor of GC, not only blocked completely the relaxation of HIMA, but also enhanced the vascular contraction induced by norepinephrine. TEA (1 mmol/L), an antagonist of calcium activated potassium channels (K(Ca)), reduced but not completely blocked the vasorelaxing effect of VNP. These findings suggest that VNP can relax HIMA, which is independent of the endothelium. This effect is possibly achieved by the binding of VNP with the natriuretic peptide GC receptors in the smooth muscle cells (SMCs), leading to an increase in intracellular cGMP level. Moreover, the vasorelaxing effect of VNP is associated with K(Ca).

Inhibition of moderate hypoxia-induced protein synthesis by vasonatrin peptide in cultured neonatal rat cardiomyocytes / 生理学报

The present work was to investigate the effects of vasonatrin peptide (VNP) on cardiomyocyte protein synthesis induced by moderate hypoxia. In cultured neonatal rat cardiomyocytes, MTT methods, total protein measurement and (3)H-leucine incorporation were used to calculate the cell number and measure the protein synthesis of cardiomyocytes. Furthermore, radioimmunoassay was undertaken to observe the effects of VNP on the intracellular levels of cAMP, cGMP and the concentration of endothelin (ET) in the culture medium. The results showed that both the cell number and protein synthesis decreased with severe hypoxia for 24 h. In contrast, under moderate hypoxia, cardiomyocyte hypertrophy developed; the protein synthesis as evidenced by total protein content and 3H-eucine incorporation increased significantly. VNP reduced cardiomyocyte protein synthesis induced by moderate hypoxia in a dose-dependent manner. Furthermore, VNP increased the intracellular level of cGMP and decreased the concentration of ET in the culture medium under moderate hypoxia, but had no effect on the level of cAMP. These results suggest that VNP inhibits moderate hypoxia-induced protein synthesis in cultured neonatal rat cardiac myocytes. This effect is mediated, at least in part, by an increase in intracellular cGMP, a reduction in synthesis, and/or a release in ET of cardiomyocytes.