Purpose:To study the effect of NVB in the treatment of advanced non small cell lung cancer (NSCLC).Methods:In 39 cases advanced stage, primary chemotherapy patients account for 30 cases and 9 were recurrent diseases.Results:CR 2 cases PR 20 cases NC 13 cases and PD 4 cases, total response rate 56.4%. The majory toxicity was bone marrow suppression.Conclusions:Combined chemotherapy including NVB has better curative effect for advanced NSCLC.

Objective To investigate the therapeutic effects of Saussurea involucrate injection in severe acute pancreatitis (SAP) in rats.Methods A total of 80 healthy Sprague-Dawley rats were divided into eight groups:SAP group (three hours、48 hours),Saussurea involucrate treated group (three hours、48 hours),ulinastatin control group (three hours、48 hours) and sham operation group (three hours、48 hours),10 rats in each group.After modeling,the rats of SAP group were regularly feeded and the rats of other three group were treated with Saussurea involucrate injection (1.04 mL/kg) intraperitoneal injection,ulinastatin 10 000 U/L tail vein injection,and saline femoral vein injection,respectively and injected every 12 hours.At three hours and 48 hours after treated,blood and pancreatic tissue samples were obtained.The mortality rate,serum amylase level and pathological changes of the pancreas of each group were observed.Serum tumor necrosis factor alpha (TNF-α),interleukin (IL)-6 and IL-10 levels were detected by enzyme linked immunosorbent assay (ELISA).The content of malondialdehyde (MDA) in pancreatic tissues was determined by chemical colorimetry.The level of TNF-α mRNA,IL 6 mRNA and IL-10 mRNA in pancreatic tissues were measured with reverse trascription-polymerase chain reaction (RT-PCR).The activity of nuclear factor kappa B p65 (NF-κB p65) in the pancreatic tissue was tested by immunohistochemistry.Single factor analysis of variance was used to compare multiple groups,and the least significant difference (LSD) method was used in the multiple comparisons between groups.Fisher's exact probability method was performed for rates comparison.Results At 48 hours,there was no statistically significant difference in mortality rate among Saussurea involucrate treated group,SAP group and ulinastatin groups (all P＞0.05).At 48 hours,the histopathology score (8.13 ± 0.64),levels of serum amylase ((2 597.0±214.0) U/L),TNF-α ((254.4±11.6) ng/L),IL-6 ((441.4±14.6) ng/L),levels of pancreatic tissues MDA ((311.0±10.6) mmol/L),TNF-α mRNA(2.04±0.08),IL-6 mRNA (1.77±0.04)and activity of NF-κB p65 ((25.90±2.90)％) of Saussurea involucrate treated group were all lower than those of SAP group (11.40±0.89,(4 780.0±101.0) U/L,(396.0±7.4) ng/L,(664.4± 7.6) ng/L,(418.0± 10.6) mmol/L,2.94±0.03,2.63±0.08 and (51.60±5.27) ％;however level of serum IL-10 ((133.5±6.9) ng/L vs (95.1±5.2) ng/L) and IL-10 mRNA of the pancreatic tissue (1.38±0.06 vs 0.85±0.03) significantly increased (F=253.07、441.63、489.40、2 465.00、196.65、477.89、562.79、131.70、560.18、570.04,all P＜0.01).There was no significant differences in all above parameters between Saussurea involucrate treated group and ulinastatin groups (7.56±0.88,(2 607.0±239.0) U/L,(252.2 ±9.2) ng/L,(443.4±9.6) ng/L,(308.4±9.2) mmol/L,2.10±0.12,1.74±0.04,(26.00±3.67)％,(134.5±7.8) ng/L and 1.42±0.06) at 48 hours (all P＞0.05).Conclusion Saussurea involucrate injection can eliminate oxygen free radicals and prevent to xidation,inhibit NF-κB activation,regulate synthesis and release of cytokines,and alleviate pancreatic injury in SAP rats,but it can not decrease mortality.

Objective:To investigate the expression of Per2 mRNA, HDAC1 mRNA and E-cadherin mRNA in esophageal cancer cells and their significance.Methods:The experimental study was conducted. Human normal esophageal epithelial cells as the control group and human esophageal cancer cell line KYSE-150 cells as the experimental group were cultured in vitro to logarithmic growth stage. Observation indicators: (1) the proliferation of cells; (2) the migration and invasion of cells; (3) the expression of Per2 mRNA, HDAC1 mRNA, and E-cadherin mRNA in cells of initial physiological state; (4) the expression of Per2 mRNA, HDAC1 mRNA, and E-cadherin mRNA after cells were treated with Per2-agonists or inhibitors; (5) the expression of Per2 mRNA and E-cadherin mRNA after cells were treated with HDAC1 inhibitors. Measurement data with normal distribution were represented as Mean± SD, the t test was used for comparison within groups and the t test or ANCOVA were used for comparison between groups. Results:(1) The proliferation of cells: the cell proliferation of the experimental group and control group were 0.90%±0.14% and 0.52%±0.08%, with a significant difference between the two groups ( t=5.166, P<0.05). (2) The migration and invasion of cells: the numbers of cell migration and invasion for the experimental group were 173±41 and 86±27, versus 50±15 and 21±9 for the control group, with significant differences between the two groups ( t=6.274, 5.153, P<0.05). (3) The expression of Per2 mRNA, HDAC1 mRNA, and E-cadherin mRNA in cells of initial physiological state: the expression of Per2 mRNA, HDAC1 mRNA, and E-cadherin mRNA in cells of initial physiological state for the experimental group was 11.7±2.7, 20.4±6.6, and 12.4±2.5, respectively, versus 2.4±0.5, 8.5±2.2, and 27.3±4.5 for the control group, with significant differences between the two groups ( t=5.782, 2.982, -5.034, P<0.05). (4) The expression of Per2 mRNA, HDAC1 mRNA, and E-cadherin mRNA after cells were treated with Per2-agonists or inhibitors: after cells were treated with Per2-agonists, the expression of Per2 mRNA, HDAC1 mRNA, and E-cadherin mRNA were 13.1±2.2, 22.4±6.2, 16.6±4.2 for the experimental group, and 9.9±3.1, 18.4±5.6, 15.3±2.3 for the control group, respectively. There was no significant difference in the expression of Per2 mRNA, HDAC1 mRNA, or E-cadherin mRNA of the experimental group between cells being treated with and without Per2-agonists ( t=-4.300, 10.087, -4.187, P>0.05). There were significant differences in the expression of Per2 mRNA, HDAC1 mRNA, and E-cadherin mRNA of the control group between cells being treated with and without Per2-agonists ( t=-4.846, 3.501, 9.294, P<0.05). There was no significant difference in the expression of Per2 mRNA or E-cadherin mRNA between the experimental group and control group after cells were treated with Per2-agonists ( F=1.000, 7.582, P>0.05), while there was a significant difference in the expression of HDAC1 mRNA between the two groups ( F=1.724, P<0.05). After cells were treated with Per2-inhibitors, the expression of Per2 mRNA, HDAC1 mRNA, and E-cadherin mRNA were 4.1±1.7, 7.5±2.2, 22.8±4.2 for the experimental group, and 3.1±0.9, 9.3±3.2, 28.4±5.8 for the control group, respectively. There were significant differences in the expression of Per2 mRNA, HDAC1 mRNA, and E-cadherin mRNA of the experimental group between cells being treated with and without Per2-inhibitors ( t=12.124, 5.105, -10.245, P<0.05). There was no significant difference in the expression of Per2 mRNA, HDAC1 mRNA, or E-cadherin mRNA of the control group between cells being treated with and without Per2-inhibitors ( t=-2.815, 1.568, -1.439, P>0.05). There were significant differences in the expression of Per2 mRNA and E-cadherin mRNA after cells were treated with Per2-inhibitors between the experimental group and control group ( F=22.965, 82.134, P<0.05), while there was no significant difference in the expressions of HDAC1 mRNA between the two groups ( F=6.416, P>0.05). (5) The expression of Per2 mRNA and E-cadherin mRNA after cells were treated with HDAC1 inhibitors: after cells were treated with HDAC1 inhibitors, the expression of Per2 mRNA and E-cadherin mRNA were 13.4±3.5, 24.2±3.4 for the experimental group, and 3.1±1.2, 26.8±5.2 for the control group, respectively. There was no significant difference in the expression of Per2 mRNA of the experimental group between cells being treated with and without HDAC1-inhibitors ( t=-3.959, P>0.05). There was a significant difference in the expression of E-cadherin mRNA of the experimental group between cells being treated with and without HDAC1-inhibitors ( t=-21.977, P<0.05). There was no significant difference in the expression of Per2 mRNA or E-cadherin mRNA of the control group between cells being treated with and without HDAC1-inhibitors ( t=-1.440, 1.058, P>0.05). After cells were treated with HDAC1-inhibitors, there was no significant difference in the expressions of Per2 mRNA between the experimental group and control group ( F=2.004, P>0.05), while there was a significant difference in the expression of E-cadherin mRNA between the two groups ( F=325.800, P<0.05). Conclusions:Human esophageal cancer cells have an elevated expression of Per2 mRNA and HDAC1 mRNA, and a reduced expression of E-cadherin mRNA. The overexpression of Per2 mRNA may activate the expression of downstream targeting protein HDAC1, and inhibit the expression of cell surface E-cadherin mRNA.