Phosphoinositide 3-kinase/Akt and nuclear factor-kappaB are involved in Staphylococcus aureus-induced apoptosis in U937 cells / 中国医学科学杂志(英文版)

<p><b>OBJECTIVE</b>To explore the mechanisms involved in Staphylococcus aureus (S. aureus) invading human monocytic U937 cells.</p><p><b>METHODS</b>S. aureus were added to U937 cells at multiplicity of infections (MOI) of 20:1 for 0, 15, 30, 60, and 90 minutes, respectively. Cell apoptosis was analyzed with Hoechst 33258 staining and Annexin V-fluorescein isothiocyanate (FITC)/propidium iodide (PI) flow cytometry analysis. Akt and nuclear factor-kappaB (NF-kappaB) activities were detected by Western blotting.</p><p><b>RESULTS</b>Infection of U937 cells with S. aureus induced rapid cell death in a time-dependent manner, and the cells displayed characteristic features of apoptosis. S. aureus-induced apoptosis was associated with a prominent downregulation of activated (phosphorylated) Akt and NF-kappaB. The inhibition of phosphorylated Akt by LY294002 led to the inhibition of NF-kappaB in a dose-dependent manner. Inhibition of Akt with LY294002 caused further increase in apoptosis of U937 cells.</p><p><b>CONCLUSIONS</b>S. aureus can stimulate the apoptosis of U937 cells. S. aureus induces apoptosis of U937 cells by inhibiting Akt-regulated NF-kappaB.</p>

C-jun N-terminal kinase-mediated signaling is essential for Staphylococcus aureus-induced U937 apoptosis / 中国医学科学杂志(英文版)

<p><b>OBJECTIVE</b>To investigate the effect of SP600125, a specific c-jun N-terminal protein kinase (JNK) inhibitor, on Staphylococcus aureus (S. aureus)-induced U937 cell death and the underlying mechanism.</p><p><b>METHODS</b>The human monocytic U937 cells were treated with S. aureus at different time with or without SP600125. Cell apoptosis was analyzed by flow cytometry. JNK, Bax, and caspase-3 activities were detected by Western blotting.</p><p><b>RESULTS</b>S. aureus induced apoptosis in cultured U937 cells in a time-dependent manner. Expression of Bax and phospho-JNK significantly increased in S. aureus-treated U937 cells, and the level of activated caspase-3 also increased in a time-dependent manner. Inhibition of JNK with SP600125 significantly inhibited S. aureus-induced apoptosis in U937 cells.</p><p><b>CONCLUSIONS</b>S. aureus can induce apoptosis in U937 cells by phosphorylation of JNK and activation of Bax and caspase-3. SP600125 protects U937 cells from apoptosis induced by S. aureus via inhibiting the activity of JNK.</p>

Involvement of p38 mitogen-activated protein kinase in E. coli-induced U937 apoptosis / 中国医学科学杂志(英文版)

<p><b>OBJECTIVE</b>To investigate whether the effect of E. coli on U937 cell lines apoptosis is mediated via p38 mitogen-activated protein kinase (MAPK) activation.</p><p><b>METHODS</b>The U937 cell lines were treated with E. coli at different time or together with SB203580, an inhibitor for p38. Cell apoptosis was analyzed by flow cytometry. p38 activities were detected by Western blotting.</p><p><b>RESULTS</b>E. coli induced apoptosis in cultured U937 cell lines in a time-dependent manner. The phosphorylation of p38 was induced after 10 minutes infection, reached the peak after 20 minutes, and started to decline after 30 minutes. In contrast, the level of total p38 protein was not changed in whole experimental period. Inhibition of p38 with SB203580 significantly inhibited E. coli induced apoptosis in U937 cells.</p><p><b>CONCLUSION</b>The activation of the p38 MAPK in U937 cell lines by E. coli is a major pathway to mediate the apoptosis.</p>

Hepatocyte growth factor protects against apoptosis induced by advanced glycation end products in endothelial cells / 中国医学科学杂志(英文版)

<p><b>OBJECTIVE</b>To investigate the effects of hepatocyte growth factor (HGF) on vascular endothelial cells apoptosis induced by advanced glycation end products (AGEs) and its possible mechanism.</p><p><b>METHODS</b>Human umbilical vein endothelial cells (HUVECs) were cultured in vitro and intervened by different concentrations of AGEs and HGF. The cell inhibitory rates of each group with different culture time (12, 24, 48, and 72 hours) were measured by methyl thiazolyl tetrazolium (MTT) assay. The early stage apoptosis was detected by flow cytometry with Annexin V-FITC/PI double staining, morphology of cell apoptosis was observed by hoechst 33258 fluorescence staining, and the expression of apoptosis-associated genes Bax and Bcl-2 were determined by Western blotting. The activity of caspase-3 was detected by enzyme-linked immunosorbent assay (ELISA).</p><p><b>RESULTS</b>Morphological observation indicated that high concentration of AGEs induced characteristic apoptotic changes in HUVECs. Within a certain concentration range, HUVECs apoptosis inducing rates by AGEs were in both dose- and time-dependent manners. HGF significantly inhibited the apoptosis of HUVECs induced by AGEs (P < 0.05). AGEs significantly promoted expression of Bax protein, but not Bcl-2. Whereas HGF significantly promoted the expression of Bcl-2 (P < 0.01) and decreased the activity of caspase-3 (P < 0.05) without affecting Bax level.</p><p><b>CONCLUSIONS</b>AGEs can induce the apoptosis of endothelial cells in vitro. HGF may effectively attenuate AGEs-induced endothelial cells apoptosis through upregulating Bcl-2 gene expression and inhibiting caspase-3 activation.</p>

Effects of positive end-expiratory pressure on pulmonary shunt during geneal anesthesia and after the operation / 中华麻醉学杂志

The effects of positive end-expiratory pressure (PEEP) on pulmonary shunt were studied during gen- eral anesthesia and postoperative period.Twenty cholecystectomy patients were randomly divided into experiment group (group P) and control group (group Z). PEEP and ZEEP were used separately after induction. Artery blood and mixed blood from the right ventricle were taken for blood gas analysis and determine the amount of pulmonary shunting before anesthesia. half and hour, one and half an hour and two and half an hour after anesthesia and one hour after the operation.The results showed that shunt in group P decreased gradually during general anesthesia and returned to the level of preoperation at an hour after operation. Shunt in group Z was increased continually and the level was significantly higher than preoperation an hour after operation. Shunt between two groups was significant difference (P

Intrapulmonary shunting during sodium nitroprusside-induced hypotension in patients undergoing nasoendoscopic operation / 中华麻醉学杂志

Objective To investigate the changes in intrapulmonary shunting during controlled hypotension induced by sodium nitroprusside(SNP)in patients undergoing naso-endoscopic operation.Methods Forty ASAⅠorⅡpatients of both sexes(23 male,17 female)aged 16-50 yrs weighing 50-75 kg undergoing naso-endoscopic operation under general anesthesia with muscle relaxation and mechanical ventilation were studied.Radial artery was cannulated for direct BP monitoring and blood sampling.Right internal jugular vein was cannulated and the catheter was advanced into right ventricle.Blood sample taken from right ventricle was used as mixed venous blood instead of blood from pulmonary artery.ECG,MAP,HR and P_(ET) CO_2 were continuously monitored during operation Cardiac output was monitored with noninvasive cardiac function monitor(NC-COM.)based on impedance principle.SNP infusion was started at the beginning of operation at 1-3?g?kg~(-1)?min~(-1) and was then adjusted.MAP was reduced by 30%-40% and maintained at this level until the end of operation.Blood samples were taken from artery and right ventricle simultaneously before SNP infusion(T_1,baseline)at 30 and 60 min of hypotension(T_2,T_3)and at 20 min after BP returned to the baseline level(T_4)for blood gas analysis.Qs/Qt was calculated.Results Qs/Qt was significantly increased during controlled hypotension at T_2 and T_3 as compared to the baseline value(P＜0.01)and returned to the baseline level at T_4.HR was increased and cardiac output and stroke volume was significantly reduced during hypotension as compared to the baseline value.Conclusion The intrapulmonary shunting is increased and the hemodynamics is depressed during SNP-induced controlled hypotension and they return rapidly to baseline level after SNP is discontinued.No hypoxemia develops during SNP- induced hypotension.