Laparoscopic versus open surgery for D2 gastrectomy in advanced gastric cancer / 中华胃肠外科杂志

<p><b>OBJECTIVE</b>To investigate the safety and feasibility of laparoscopic D2 gastrectomy for advanced gastric cancer.</p><p><b>METHODS</b>The clinical data of 210 cases of laparoscopic gastrectomy and 180 cases of open gastrectomy for radical (D2) gastrectomy from May 2007 to Dec 2010 were analyzed retrospectively.</p><p><b>RESULTS</b>A total of 206 cases underwent laparoscopic-assisted surgery with 4 conversions. Compared to the open group, the laparoscopic group was associated with less bleeding [(208±38) ml vs. (300±52) ml, P<0.05], quicker postoperative recovery of bowel function [(2.9±0.7) d vs. (3.9±1.8) d, P<0.05], shorter postoperative length of hospital stay[(12.8±6.2) d vs. (15.6±6.8) d, P<0.05], longer operative time [(258±42) min vs. (193±30) min, P<0.05]. The number of lymph node harvested was 20.5±1.9 in the laparoscopic group and 25.8±1.5 in the open group, and the postoperative complication rate was 8.1% (17/201) vs. 8.5% (15/180), and differences were not statistically significant (both P>0.05). The recurrence rate was 2.9% (6/210) and 2.8% (5/180), and the 3-year overall survival rate was 35.6% and 37.8%, the differences were not statistically significant (both P>0.05).</p><p><b>CONCLUSIONS</b>Laparoscopic radical gastrectomy for gastric cancer is safe and effective, which can reach the same range of lymph node dissection as open gastric cancer surgery and similar survival rate.</p>

Ginsenoside Rbl attenuates beta-amyloid peptide25-35 -induced tau hyperphosphorylation in cortical neurons / 药学学报

<p><b>AIM</b>To explore the effect and the possible mechanism of ginsenoside Rb1 on beta-amyloid peptide (beta-AP)(25-35) -induced tau protein hyperphosphorylation in cortical neurons.</p><p><b>METHODS</b>Western blotting and immunocytochemical staining were used to detect tau phosphorylation level, total tau and glycogen synthase kinase-3beta (GSK-3beta) in cortical neurons.</p><p><b>RESULTS</b>After exposure to beta-AP(25-35) (20 micromol x L(-1)) for 12 h, the levels of tau protein phosphorylation in the sites of Ser 396, Ser 199/202, Thr 231 and total tau were raised. Meanwhile, the expression of GSK-3beta also increased. Pretreatment with ginsenoside Rbl or lithium chloride, a specific inhibitor of GSK-3beta, markedly reduced beta-AP(25-35)-induced tau hyperphosphorylation and the expression of GSK-3beta.</p><p><b>CONCLUSION</b>Ginsenoside Rb1 can attenuate beta AP(25-35)-induced tau protein hyperphosphorylation in cortical neurons by inhibiting the expression of GSK-3beta.</p>

Ginsenoside Rb1 attenuates okadaic acid-induced Tau protein hyperphosphorylation in rat hippocampal neurons / 生理学报

The present study was aimed to investigate the effects of ginsenoside Rb1 on okadaic acid (OA)-induced Tau hyperphosphorylation in hippocampal neurons of Sparague-Dawley rat and to explore its possible mechanism. Animals were randomly divided into four groups. Group 1 received dimethysulphoxide (DMSO) injection (vehicle group), group 2 only received OA injection (OA group), group 3 was pretreated with Rb1 and then received OA injection (Rb1 pretreatment group), and the group 4 was an intact control group. The animals in group 3 were injected intraperitoneally with various doses of Rb1 at 5, 10, and 20 mg/kg (once a day for 14 d). On the thirteen day of pretreatment, animals in Rb1 pretreatment group as well as animals in OA group received a bolus injection of 0.483 microg of OA (1.5 microl of solution in DMSO) at right dorsal aspect of hippocampus to induce Tau hyperphosphrylation. The brains were harvested one day after the last treatment. In all groups, the morphology of neurofibrils, phosphorylation of Tau protein, and the activity of phosphatase 2A (PP2A) were investigated. In OA group, the Bielschowski's assay revealed darkened and uneven neurofibrils staining in the hippocampus. The immunohistochemistry results showed a significant increase in Thr(231) phosphorylation of Tau protein in OA group relative to the control group (P<0.01). OA injection also markedly decreased PP2A activity (P<0.01). Western blot confirmed Thr(231) phosphorylation of Tau protein and it also detected phosphorylation of Ser(396) of Tau protein. The animals with Rb1 pretreatment displayed even staining of neurofibrils and normal pattern of fiber organization. Rb1 pretreatment also attenuated Thr(231) and Ser(396) hyperphosphorylations of Tau protein, and restored PP2A activity compared to the OA group (P<0.01). These results indicate that OA-induced hyperphosphorylation of Tau protein in rat hippocampal neurons can be attenuated by the pretreatment of ginsenoside Rb1. These data also implicate that Rb1 has potential neuroprotective effects on Tau-related neuropathology.

Effect of ginsenoside Rg1 on expression of p21, cyclin E and CDK2 in the process of cell senescence / 药学学报

<p><b>AIM</b>To explore the possible role of p21, cyclin E and cyclin-dependent kinase 2 (CDK2) in the protection of ginsenoside Rg1 against tert-butylhydroperoxide (t-BHP)-induced senescence in WI-38 cells.</p><p><b>METHODS</b>The cellular ultrastructure, cytometric assay and beta-galactosidase (beta-gal) cytochemistry staining were used to evaluate cell senescence. The levels of of p21, cyclin E and CDK2 protein were detected by Western blot.</p><p><b>RESULTS</b>Pretreatment with Rg1 significantly attenuated t-BHP-induced senescence in WI-38 cells. Simultaneously, compared with cells treated with t-BHP alone, Rg1 pretreatment markedly decreased the level of p21 protein and increased the levels of CDK2 and cyclin E.</p><p><b>CONCLUSION</b>p21, cyclin E and CDK2 may be involved in the process of ginsenoside Rg1 protection against t-BHP-induced senescence in WI-38 cells.</p>