Purpose To explore the expression of thioredoxin reductase-1 ( TrxR1 ) in non-small cell lung cancer and to observe the effects of TrxR1 on non-small cell lung cancer ( NSCLC) . Methods Immunohistochemistry was used to determine the expression of TrxR1 in 118 NSCLC tissues and 27 normal lung tissues, and to analyze its relationships with clinical pathological features. TrxR1 mR-NA levels were measured by quantitative RT-PCR in 13 cases of NSCLC and 4 cases of normal lung tissue. TrxR1 protein and its mR-NA levels were assessed by Western blotting and quantitative RT-PCR in normal lung epithelial cells and different lung cancer cell lines. After the silence TrxR1 expression in A549 cells, the changes of proliferation were compared. Results The data of immunohis-tochemistry and quantitative RT-PCR showed the overexpression of TrxR1 in NSCLC ( P <0. 05 ) . After using shRNA silencing of TrxR1 in lung cancer cells, cell proliferation changed significantly. Conclusion There are a high mRNA and protein levels of TrxR1 in NSCLC. TrxR1 may be a critical therapeutic target for the treatment in NSCLC.

Objective To investigate the early enteral nutrition (EN) and total parenteral nutrition (TPN) on the periopera‐tive nutritional status of gastric cancer patients underwent total gastrectomy .Methods 96 cases of total gastrectomy for gastric cancer patients treated in our hospital from January 2011 to March 2013 were randomly assigned ratio EN group and the TPN group ,with 48 cases in each group;nutritional status were compared before and after treatment .Results EN group was superior in nutritional status than TPN group ,it had shorter recover time and less complications (P<0 .05) .Conclusion Early enteral nutri‐tion support can quickly restore the nutritional status of patients and improve the immune status .

Objective To investigate the protective effects of recombinant human tumor necrosis factor receptor:Fc fusion protein (rhuTNFR:Ice)on the acute renal injury induced by lipepelysaccharide(LPS)in rats.Methods Models ofacute renal injury in rats were constructed by intravenous injection of LPS 10 m/kg.Forty-eight SD rats weighing 180～240g were randomly divided into 4 groups with 12 animals each group,including control group,rhuTNFR:Fc group,LPS groupand rhuTNFR:Fc+LPS group.Mean arterial pressure(MAP)wKs continuously monitored for 6 h.The levels of blood tLrea nitrogen(BUN)。Creatinine(Cr),TNF-αas well as TNF-α bioactivity were assessed.The myeloperoxinse(MPO)and superoxide dismutase(SOD)activity,content ofmalondialdehyde(MDA)were also measured.Pathologic changes of lung tissue in each group were observed by HE staining.Results Compared with LPS group,the status of hypotension and pathological manifestation in kidneys were ameliorated,and MPO activity significantly decreased in rhuTNFR:Fc+LPS group(P<0.05).Conclusion These data suggest that rhuTNFR:Fc can ablate the rise in serum TNF-α bioactivity that occurs in response to LPS,and rhuTNFR:Fc could in part protect rats from the acute renal injury induced by LPS.

Objective To investigate the protective effects and the undedying mechanism of recombinant human tumor necrosis factor receptor: Fc fusion protein (Yisaipu, rhu TNFR: Fc) on the lipopolysaccharide (LPS) induced acute liver injury of rats. Method Totally48 SD rats were randondy divided into four groups , in-cluding control gronp (n = 12), Yisaipu group(n = 12), LPS gronp(n = 12) and Yisaipu + IPS group(n = 12). The models of acute liver injury were produced by injection of LPS intravenously. Being fasted for 12 h, the rats were anaesthetized (60 mg/kg pentobarbital sodium, i.p.) and cannulated into carotid arteries. The cannula was connected with the multi-channel creature signal analysis system. The rata in control group and LPS group were injected with normal saline or LPS in dose of 5 mg/kg through rats' sublingual vein respectively. While the rats in Yisaipu group and Yisaipu + LPS group was pretreated with Yisaipu in dose of 0.4 mg/kg subcutaneously 24 h be-fore normal saline or LPS infusion. Six rats of each goup were randomly selected and mean arterial pressure (MAP) were monitored for 6 h via multi-channel creature signal analysis system, and rats' survival rate was calcu-lated. The rats whose MAP less than 10 mmHg were considered to die and the alive rats during period of observa-tion sacrificed by exsanguination. The liver tissue at the same site was removed, fixing in 10% formalin or stored at -80 ℃. To detect serum TNF-α, alanine aminotransferase (ALT) and aspartate aminotransferase (AST) level, 0.2 mL blood samples were collected from the carotid artery 2 and 3 h after the injection of saline or LPS. The serum was collected from centrifuged blood samples and stored at -80 ℃. Enzyme-linked immunosorbent assay (ELISA) and flow cytometry were used to assess serum TNF-α level and bioactivity respectively. We also measured the serum ALT and AST levels, the myeloperoxiase (MPO) and superexide dismutase (SOD) activity, and malon-dialdehyde (MDA) content in liver tissue The pathology of hepatic tissue was evaluated by HE staining. Statistical-ly,the data of TNF-α level and bioactivity, ALT and AST release, and MDA content were analyzed by ANOVA, and rat survival rate were analyzed by Chi-square Tests. Results The rats in control group and Yisaipu group were all survived. Rat survival rate was significantly higher in Yisaipu + LPS group (67%) than in LPS group (17%) (P < 0.05). Serum TNF-α bioactivity was significantly lower in Yisaipu + LPS group than in LPS group [(7.3±2.8)% vs.(51.3±6.4)%, P <0.05]. Compared with IPS group, Yisaipu pretreatment decreased MDA content [(1.40±0.10)vs. (2.81±0.11) nmol/mgprot, P <0.05]and MPO acticity [(0.38±0.04) vs. (0.54±0.02) U/g, P <0.05]in hepatic tissue, while SOD activity [(188.4±20.2) vs. (142.5 ± 18.3) U/mgprot, P <0.05]was increased. The serum AST level, ALT level and the pathology in the liver were also ameliorated correspondingly. Conclusions These data suggest that Yisaipu could protect rats from LPsinduced a-cute liver injury by inhibiting TNF-α bioactivity and by enhancing anti-oxidation.

Objective To investigate the role of calcitonin gene-related peptide(CGRP)and IP3 signal pathway in ischemic preconditioning(IPC)in the isolated perfused hearts of rats with type 1 diabetes mellitus. Methods Type 1 diabetes mellitus rat models were established in 80 SD rats,and were randomly divided into 4 week(D-4w)group and 8 week (D-8w)group.These two groups were randomly subdivided into model control(D-Cont)group,type 1 diabetes mellitus ischemia-reperfusion(IR)group,IPC group,CGRP(IPC+CGRP)group and IP3 inhibitor wortmanin(IPC+WMN) group.Another 16 rats were served as normal control(N-Cont)group.In vitro perfusion models of isolated hearts were established by Langendorff methods,and CGRP or wortmanin(WMN)were administered during perfusion.The left ventricle function of isolated heart in each group was monitored by multichannel biosignal analysis system,and coronary artery flow was recorded.The serum CGRP levels were detected by ELISA.The activity of lactate dehydrogenase(LDH)and creatine kinase(CK)in effluent of coronary artery was detected by biochemical method.The size of myocardial infarction was determined by NBT staining,and apoptosis of cadiocytes was detected by TUNEL method. Results Compared with N- Cont group,the CGRP level in serum of rats with type 1 diabetes mellitus decreased with time,the basic left ventricle function decreased,while the activity of LDH and CK in effluent of coronary artery,size of myocardial infarction and cardiomyocyte apoptosis index increased(P<0.05).Compared with N-Cont group,the left ventricle function was significantly lower in IR group,and more severe myocardial damage was observed.IPC improved myocardial damage of D-4w IR group,while had no protection on D-8w IR group.Compared with IPC group,the left ventricle function was significantly improved in IPC+CGRP group.IPC+WMN blocked the myocardial protection of D-4w group from IPC.Conclusion CGRP and IP3 signal pathway are involved in the protection provided by IPC in isolated hearts of rats with type 1 diabetes mellitus.