Zuo-Bing Chen

Allicin, a major component of garlic, inhibits apoptosis in vital organs in rats with trauma/hemorrhagic shock*

Objective:Allicin is believed to be the main component responsible for the biological activity of garlic. The regulation of cell apoptosis may have therapeutic potential for trauma/hemorrhagic shock, and previous studies have demonstrated that allicin exerts protective effects against tissue ischemia-reperfusion injury. Therefore, this study examined the effects of allicin on apoptosis-related organ damage, induced by trauma/hemorrhagic shock. Methods:Studies were performed on an in vivo model of spontaneously breathing rats with induced trauma/hemorrhagic shock; the left lower lobe of the lungs, left kidney, and intestine were resected, and the rats were subjected to femur fracture, ischemia for 30 mins, and reperfusion for 20 mins. Allicin (30 &mgr;g/kg) was administered during reperfusion. Results:Allicin administered during reperfusion markedly attenuated injury and apoptosis of the lungs, kidneys, and intestine and decreased the concentrations of lactic acid and creatinine, the number of in situ TdT-mediated dUTP nick-end labeling-positive cells, and the activity and expression of caspase-3 and -9 (as determined by Western blot). Furthermore, immunohistochemistry and Western blot performed 24 hrs after reperfusion revealed increases in the levels of nuclear factor &kgr;B, phosphorylated p38, and extracellular signal-regulated kinase 1 mitogen-activated protein kinase in the allicin-untreated group when compared with the sham rats. Allicin treatment downregulated the levels of nuclear factor &kgr;B and phosphorylated p38 mitogen-activated protein kinase but did not modify those of phosphorylated extracellular signal-regulated kinase 1 mitogen-activated protein kinase. Conclusion:Allicin attenuates tissue injury and inhibits trauma/hemorrhagic shock- and reperfusion-induced apoptosis in several important organs via the p38 mitogen-activated protein kinase signal transduction pathway that functions to stimulate the activation of nuclear factor-&kgr;B, caspase-3 and -9, but not of extracellular signal-regulated kinase 1 mitogen-activated protein kinase.

Resuscitation with hydroxyethyl starch solution prevents CD4+ T-lymphocyte apoptosis and modulates the balance of T helper type 1 and T helper type 2 responses in the rat with traumatic virgule/shill hemorrhagic shock.

Trauma/hemorrhagic shock (TH/S) has been associated with inflammation and immunodisorders, leading to immunosuppression, multiorgan dysfunction, and death. However, little is known about the effect of resuscitation with different solutions on the immunological function. To address this issue, groups of male Sprague-Dawley rats were induced with TH/S by fracture in the left femur and continual bleeding to keep the MAP of 30 ± 5 mmHg for 30 min, followed by resuscitation with 6% hydroxyethyl starch solution (HES), Ringers lactate solution (RS), or 5% albumin (ALB), and the impact of resuscitation on the activation, differentiation, and survival of CD4+ T cells was longitudinally examined after TH/S and resuscitation. After resuscitation, the MAP, as expected, gradually increased regardless of the type of fluids transfused. The percentage of CD4+ T cells decreased to 20% to 25%, and the ratio of T helper type 1 (TH1)/TH2 responses was significantly reduced in all TH/S rats, however, resuscitation with HES alone reversed the trends (49.4% ± 9.7% vs. 55.2% ± 2.6% in sham for CD4+ T cells; 0.64 ± 0.23 vs. 0.71 ± 0.16 in sham for the ratio of TH1/TH2, P > 0.05 for both). Treatment with HES or ALB, but not RS, prevented CD4+ T-cell apoptosis (sham, 7.23% ± 3.4%; HES, 10.2% ± 4.1%; RS, 15.2% ± 5.4%; ALB, 10.6% ± 4.3%; 48 h) and nuclear factor-&kgr;B p65 activation (sham, 0.17 ± 0.04; HES, 0.34 ± 0.05; RS, 0.41 ± 0.09; ALB, 0.25 ± 0.09; 48 h) induced by TH/S early after resuscitation. These data demonstrated that HES resuscitation modulated the balance of TH1 and TH2 responses and inhibited TH/S-related nuclear factor-&kgr;B activation and CD4+ T-cell apoptosis in TH/S rats. Our findings provide new insights into understanding the TH/S-related immunodisorders and may aid in the design of new therapy for intervention of TH/S.ABBREVIATIONS: ALB-albumin; ELISA-enzyme-linked immunosorbent assay; HES-hydroxyethyl starch solution; RS-Ringers lactate solution; TH/S-trauma/hemorrhagic shock; TH1-T helper type 1; TH2-T helper type 2

Albumin resuscitation protects against traumatic/hemorrhagic shock-induced lung apoptosis in rats.

ObjectiveTo determine the effects of albumin administration on lung injury and apoptosis in traumatic/hemorrhagic shock (T/HS) rats.MethodsStudies were performed on an in vivo model of spontaneously breathing rats with induced T/HS; the rats were subjected to femur fracture, ischemia for 30 min, and reperfusion for 20 min with Ringer’s lactate solution (RS) or 5% (w/v) albumin (ALB), and the left lower lobes of the lungs were resected.ResultsAlbumin administered during reperfusion markedly attenuated injury of the lung and decreased the concentration of lactic acid and the number of in situ TdT-mediated dUTP nick-end labelling (TUNEL)-positive cells. Moreover, immunohistochemistry performed 24 h after reperfusion revealed increases in the level of nuclear factor κB (NF-κB), and phosphorylated p38 mitogen-activated protein kinase (MAPK) in the albumin-untreated group was down-regulated by albumin treatment when compared with the sham rats.ConclusionResuscitation with albumin attenuates tissue injury and inhibits T/HS-induced apoptosis in the lung via the p38 MAPK signal transduction pathway that functions to stimulate the activation of NF-κB.

Surgical intervention of severe post-ERCP-pancreatitis accompanied with duodenum perforation.

Endoscopic retrograde cholangiopancreatography (ERCP) is a procedure widely used to diagnose and treat conditions of biliary or pancreatic ductal system. The post-ERCP severe acute pancreatitis (SAP) accompanied with duodenum perforation is rare but serious, remaining a challenge in clinic. In this study we report two such cases. Two Chinese women were treated for clinical suspicion of bile duct obstruction and underwent ERCP after admission. Both developed duodenum perforation and SAP after ERCP, and were managed in the intensive care unit (ICU) and required an organ-failure support. The surgical intervention of the peri-pancreatic debridement with lumber-abdominal compound incisions and postoperative washing and drainage was performed, and the two patients recovered well. The therapeutic effect of the peri-pancreatic debridement with lumber-abdominal compound incisions combined with postoperative washing and drainage in the patients of severe post-ERCP-pancreatitis (PEP) and duodenum perforation is satisfactory.

Early enteral nutrition with polymeric feeds was associated with chylous ascites in patients with severe acute pancreatitis.

Objective Chylous ascites (CA) may be involved in the pathological process of severe acute pancreatitis (SAP), but the underlying mechanisms remain unknown. This study investigated the incidence of CA in patients with SAP and its relationship with enteral nutrition (EN). Methods A retrospective review of 85 patients with SAP admitted to our hospital was performed. Patients starting EN within 72 hours after the onset of SAP were classified as the early EN (EEN) group, and others, as the later EN group. The incidences of CA and prognosis in the EEN and later EN groups were examined with nutrition preparation of polymeric formula or semielemental feed. Results Thirteen (15.29%) of 85 patients were identified with CA. A higher incidence of CA was observed in EEN patients who received polymeric formula (9 of 33, P < 0.05). All patients with CA were successfully treated with a modified medium-chain triglyceride diet. Consequently, there were no differences in intensive care unit stay and in mortality rates in patients with or without CA. Conclusions There was a higher incidence of CA associated with early enteral feeding of polymeric formula in patients with SAP. Future studies are warranted to confirm our findings and evaluate better enteral feeding options to avoid CA.