Clinical importance of preoperative measurement of plasma amino-terminal pro-B-type natriuretic peptide in infants with congenital heart disease / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To define cut-off values of plasma amino-terminal pro-B-type natriuretic peptide (NT-ProBNP) for the diagnosis of congenital heart failure (CHF) and evaluate the importance of plasma NT-ProBNP measurement in the assessment of cardiac function prior to heart surgery in infants with congenital heart disease (CHD).</p><p><b>METHODS</b>Plasma levels of NT-proBNP were measured in 120 infants with CHD before heart surgery and in 100 age-matched healthy infants between June 2010 and June 2013. The data were stratified based on the presence or absence of CHF in the whole group of CHD infants and on age (i.e., <1 year and ≥1 year) and time (i.e., before surgery) within the subgroup of CHF infants.</p><p><b>RESULTS</b>Of the 120 infants with CHD, 41 met the criteria for CHF defined in the Ross Classification for Heart Failure in Infants.The cut-off values of plasma NT-ProBNP were ≥498 ng/L for infants of all ages, 557 ng/L for <1 year age group and 452 ng/L for ≥1 year age group, respectively, in the 41 CHF patients. In CHF infants, plasma NT-proBNP was significantly decreased after protecting of cardiac function (P<0.001).</p><p><b>CONCLUSIONS</b>The cut-off values of plasma NT-ProBNP for CHF differ between infants <1 year and infants ≥1 year. Moreover, plasma NT-ProBNP can be used as an additional parameter in the preoperative assessment of cardiac function in CHD infants.</p>

Effect of ursolic acid on proliferation and apoptosis of hepatic stellate cells in vitro / 中华肝脏病杂志

<p><b>OBJECTIVE</b>To investigate the effect of ursolic acid on proliferation and apoptosis of hepatic stellate cells (HSC) in vitro and explore the mechanisms of apoptosis of HSC induced by ursolic acid by studying the expressions of apoptosis-regulating proteins Bcl-2, Bax and Caspase 3 in HSC.</p><p><b>METHODS</b>Hepatic stellate cells HSC-T6 and hepatocytes L02 were incubated with different concentrations of ursolic acid (25, 50, 75, 100, 125 and 150 micromol/L) for 24 h, 48 h and 72 h. The effect of ursolic acid on the cell proliferation was studied by methyl thiazolyl tetrazolium (MTT) colorimetric assay. The rate of HSC-T6 apoptosis was identified by flow cytometry (FCM) and the morphological change of apoptosis was observed with light microscopy. The expressions of apoptosis-regulating protein Bcl-2, Bax and Caspase 3 in HSC-T6 after apoptosis induced by ursolic acid were examined by immunocytochemical staining assay.</p><p><b>RESULTS</b>MTT analysis indicated administration of 25-150 micromol/L ursolic acid incubated with HSC-T6 for 24 h, 48 h and 72 h significantly inhibited HSC-T6 proliferation in a dose-dependent and time-dependent manner compared with the control group. Promotive effect of ursolic acid on proliferation of hepatocyte L02 was observed in the 25, 50, 75 micromol/L concentration groups. Ursolic acid inhibited L02 proliferation when its concentration was higher than 100 micromol/L and for 72 hours or longer. HE stained histological slides demonstrated morphologic changes of HSC-T6, including karyorrhexis and cytoplasm vacuolization, when they were treated with ursolic acid at 75 micromol/L concentrations for 48 h. FCM showed the apoptosis ratios of HSC-T6 were 10.30%+/-3.85%, 21.87%+/-4.46% and 31.33%+/-6.18% after treating HSC-T6 with ursolic acid at concentrations of 25, 50 and 75 micromol/L for 48 h. They were significantly higher than that of the control group 2.93%+/-1.60%. Immunocytochemistry also indicated the expressions of Bax and caspase 3 protein in HSC-T6 cells were up-regulated in a dose-dependent manner, but expressions of Bcl-2 protein were not significantly different from that of the blank control group (P more than 0.05).</p><p><b>CONCLUSIONS</b>Ursolic acid could significantly inhibit HSC proliferation and induce apoptosis in a dose-dependent and time-dependent manner. Ursolic acid in low concentration promotes proliferation of L02 cells, but in high concentrations (more than 100 micromol/L) it inhibits the growth of hepatocytes. Expressions of Bax and Caspase 3 in apoptotic HSC were increased; expressions of Bcl-2 protein were not significantly different from that of the control group, while Bcl-2/Bax ratio was reduced. Our results suggest that HSC-T6 cell apoptosis induced by ursolic acid occurs through mechanisms involving mitochondrial pathways and Bcl-2 family proteins.</p>

Inhibition of magnesium lithospermate B on the c-Jun N-terminal kinase 3 mRNA expression in cardiomyocytes encountered ischemia/reperfusion injury / 药学学报

<p><b>AIM</b>To study the function of c-Jun N-terminal kinase 3 (JNK3) in the process of ischemic/reperfused heart injury and the mechanism underlying the protective action of magnesium lithospermate B (MTB), a bioactive compound isolated from Danshen.</p><p><b>METHODS</b>By in situ hybridization, JNK3 mRNA was detected in the ventricular preparations of the Langendorff ischemic/reperfused rat heart. The inhibitory effect of MTB on the expression of JNK3 mRNA was also investigated.</p><p><b>RESULTS</b>The purple and blue hybridization signals were located in the cytoplasm of the cardiomyocytes, which were weaker in the non-perfused hearts and stronger in the hearts encountered 30 min of ischemia and 30 min of reperfusion. Image analysis showed that the expression of JNK3 mRNA in the cardiomyocytes increased after 30 min of ischemia and 30 min of reperfusion, which showed significant difference compared with that in the cardiomyocytes of the non-perfused heart and the control heart (P < 0.05). Treatment with of 0.1, 1 and 10 mumol.L-1 MTB abolished the elevation of JNK3 mRNA expression in the ischemic/reperfused heart (P < 0.05).</p><p><b>CONCLUSION</b>JNK3 may be another component in the signal transduction pathway of ischemia/reperfusion induced cardiomyocyte apoptosis. MTB may protect the heart from ischemia/reperfusion injury by reducing apoptosis through inhibition of the JNK3 activity.</p>