Objective To investigate the effect of Salidroside in inducing apoptosis of rat hepatic stellate cells (HSC) stimulated by acetaldehyde and to observe the changes of c- Jnk N- terminal kinase (JNK) activity.Methods HSC stimulated by acetaldehyde were cultured in vitro and were treated with different concentrations of Salidroside.Apoptotic rate was analyzed by flow cytometry and the activity of phosphorylating JNK was measured by Western blot method.Results Salidroside in different concentrations (1.0,1.5,2.0 mg/mL) suppressed the activity of JNK in a dose- effect manner.Average light density was 35.8? 3.4,24.9? 2.7 and 3.4? 0.9 in Salidroside groups, which differed from that in acetaldehyde group( 48.6? 4.8; P

Objective:Discuss and analyze the mechanisms of spine fine adjusting through the observation of the therapeutic effect in treating cervical spondylotic radiculopathy(CSR)and the conversion of cervical curvature.Methods: Randomly divide 106 CSR patients into two groups–manipulation therapy group and traction therapy group,53 for each.Judge the therapeutic effect by evaluation scales and measure the cervical curvature on X-ray photographs.Results:The symptoms and physical signs of the patients in both two groups have been improved(P

Objective To analyze the expression and role of ubiquitin specific peptidase 18 (USP18) in gastric cancer cells,and to investigate the relationship between the development of gastric cancer and USP18.Methods The levels of USP18 protein and mRNA expression in immortalized gastric mucosa epithelial GSE cell lines and gastric cancer cell lines (AGS,MKN45,MKN25,BGC823,BGC803,SGC7901) were detected by using reverse transcription-polymerase chain reaction (RT-PCR) and Western blot,respectively.The role of USP18 in the invasion and proliferation of gastric cancer cells was analyzed by using CCK8 and Transwell assays.Results The mRNA level of USP18 was lower in GSE cell lines than that in gastric cancer cells (F =794.052,P ＜ 0.000 1).In six gastric cancer cell lines,mRNA level of USP18 was relatively high in BGC823 (17.62±0.55) and BGC803 (13.52±0.50) cell lines,and low in MKN28 (1.40±0.17) and MKN45 cell lines (4.23±0.26).As for the protein level,the expression of USP18 was lowest in GSE cell line.In six gastric cancer cell lines,the expression of USP18 was the highest in more aggressive SGC7901 and BGC803 cell lines and the lowest in AGS and MKN45 cells.Compared with the control group,interference of USP18 decreased the invasion and proliferation abilities of SGC7901 and BGC803 cell lines (P ＜ 0.01).Conclusion USP18 is highly expressed in more invasive gastric cancer cells,and the downregulation of USP18 can suppress the invasion and proliferation of gastric cancer cells.

Objective To observe the effect of mild hypothermia on myocardial β-adrenergic receptor (β-AR) signal pathway after cardiopulmonary resuscitation (CPR) in pigs with cardiac arrest (CA) and explore the mechanism of myocardial protection. Methods Healthy male Landraces were collected for reproducing the CA-CPR model (after 8-minute untreated ventricular fibrillation, CPR was implemented). The animals were divided into two groups according to random number table (n = 8). In the mild hypothermia group, the blood temperature of the animals was induced to 33 ℃ and maintained for 6 hours within 20 minutes after return of spontaneous circulation (ROSC) by using a hypothermia therapeutic apparatus. In the control group, the body temperature of the animals was maintained at (38.0±0.5)℃ with cold and warm blankets. The heart rate (HR), mean arterial pressure (MAP), the maximum rate of increase or decrease in left rentricular pressure (+dp/dt max)were measured during the course of the experiment. The cardiac output (CO) was measured by heat dilution methods before CA (baseline), and 0.5, 1, 3, 6 hours after ROSC respectively, the venous blood was collected to detect the concentration of cTnI. Left ventricular ejection fraction (LVEF) was measured with cardiac ultrasound before CA and 6 hours after ROSC. Animals were sacrificed at 6 hours after ROSC and the myocardial tissue was harvested quickly, the mRNA expression of β1-AR in myocardium was detected by reverse transcription-polymerase chain reaction (RT-PCR), the contents of adenylate cyclase (AC) and cyclic adenosine monophosphate (cAMP) were detected by enzyme linked immunosorbent assay (ELISA), the protein content of G protein-coupled receptor kinase 2 (GRK2) was detected by Western Blot. Results After successful resuscitation, the HR of both groups were significantly higher than the baseline values, CO, ±dp/dt max were significantly decreased, MAP were not significantly changed, serum cTnI levels were significantly increased. Compared with the control group, HR at 0.5, 1, 3 hours after ROSC were significantly decreased in mild hypothermia group (bpm: 142.80±12.83 vs. 176.88±15.14, 115.80±11.48 vs. 147.88±18.53, 112.60±7.40 vs. 138.50±12.02, all 1 < 0.01), CO was significantly increased at 1 hours and 3 hours after ROSC (L/min: 3.97±0.40 vs. 3.02±0.32, 4.00±0.11 vs. 3.11±0.59, both 1 < 0.01), +dp/dt max at 3 hours and 6 hours was also significantly increased after ROSC [+dp/dt max (mmHg/s): 3 402.5±612.7 vs. 2 130.0±450.6, 3 857.5±510.4 vs. 2 562.5±633.9; -dp/dt max (mmHg/s): 2 935.0±753.2 vs. 1 732.5±513.6, 3 520.0±563.6 vs. 2 510.0±554.3, all 1 < 0.05], the cTnI was significantly decreased at 3 hours and 6 hours afher ROSC (μg/L: 1.39±0.40 vs. 3.24±0.78, 1.46±0.35 vs. 3.78±0.93, both 1 < 0.01). The left at 6 hours after ROSC in both groups was decreased as compared with that before CA. The LVEF in the mild hypothermia group was higher than that in the control group (0.52±0.04 vs. 0.40±0.05, 1 < 0.05). The mRNA expression of β1-AR, and concentrations of AC and cAMP in hypothermia group were significantly higher than those in control group [β1-AR mRNA (2-ΔΔCT): 1.18±0.39 vs. 0.55±0.17, AC (ng/L):197.0±10.5 vs. 162.0±6.3, cAMP (nmol/L): 1 310.58±48.82 vs. 891.25±64.95, all 1 < 0.05], GRK2 was lower than that in the control group (GRK2/GAPDH: 0.45±0.05 vs. 0.80±0.08, 1 < 0.05). Conclusion Mild hypothermia can reduce the degree of cardiac function injury after CPR, and its mechanism may be related to the reduction of impaired myocardial β-AR signaling after CPR.