It has long been acknowledged that there is a link between inflammation and cancer, but its molecular mechanism remains unclear. A key player in inflammation is nuclear transcription factor NF-?B, that activity is triggered in response to infectious agents and proinflammatory cytokines via the I?B kinase. In parenchyma cells, inflammation through I?B kinase/NF-?B pathway suppresses apoptosis, accelerates cell cycle, then promote tumorigenesis. In mesenchyma cells inflammation through I?B kinase/NF-?B pathway produces cytokines and chemokines that may serve as tumor growth factors. To sum up, I?B kinase/NF -?B pathway represents a critical molecular link between inflammation and cancer.

AIM: Three different antisense oligonucleotides complementary to basic fibroblast growth factor (bFGF) mRNA were compared in inhibitory effect on gene targeted expression. METHODS: After transfecting bFGF antisense oligonucleotides (asODN) into SWO-38 cells by lipofectin,the proliferation of cells was identified by MTT method, apoptosis was examined by flow cytometric cell cycle analysis and the expression levers of bFGF were detected by Western-blotting. RESULTS: There were 49%,33%,51% inhibition of cell growth and 35%, 27%, 18% cell apoptosis after asODN1, asODN2 and asODN3 treatment.In addition,the decrease in bFGF protein was 63%, 42%, 11%, respectively. CONCLUSION: The data suggeste that asODN1 is a potent target to bFGF mRNA, which inhibits cell growth and induces apoptosis in SWO-38 cells.

We prepared bovine epidermal keratin (EK) antibody, which can be used as a specific marker of cholangiocarcinoma(CC) cells to be distinguished from hepatocellular carcinoma (HCC) cells. The intrahepatically implanted solid tumors of FSK 7901 and FSK 7902 have the histological structures of CC and HCC, respectively. Using immunofluorescence and PAP techniques, we demonstrated that, in the solid tumors, FSK 7901 cells are definitely EK-positive, while most of the cells of FSK 7902 are EK-negative. Therefore, we considered FSK 7901 and FSK 7902 as CC and HCC, respectively. In the solid tumors of FSK 7902, few cells which are EK-positive may be those in which there are Mallory bodies or the structures are forming.

Objective: To investigate the protective effect of trimetazidine on experimental myocardial ischemia and its mechanism. Methods: Fifty mice received isoproterenol (20 mg?kg -1 ?2 d,ip) were divided into control and treatment groups. The myocyte ultrastructure,serum creatine phosphokinase (CK) activities and lactate dehydrogenase (LDH), myocardial malondialdehyde (MDA) and superoxide dismutase (SOD) were observed in 3 groups. Results: Compared with the controls,in 2 groups pretreated with trimetazidine (5 mg?kg -1 ?d -1 and 10 mg?kg -1 ?d -1 ? 7 d, ip), the degree of myocardial damage were significantly reduced;the serum CK and LDH were lower;the myocardial MDA was lower;the myocardial SOD was higher. Conclusion: Trimetazidine can significantly reduce the degree of myocardial damage produced by isoproterenol;and it may play an important role in protecting ischemic myocardium, the mechanism may be associated with reduced oxygen free radical production.

Objective:To study the protective effect of trimetazidine(TMZ) on myocardial ischemia and reperfusion injury and its mechanism.Methods:Totally 50 SD rats were randomly divided into 4 groups:the pseudooperation group,the saline group and the TMZ treated groups(5 mg?kg -1 and 10 mg?kg -1 ).In the pseudooperation group the coronary artery was not ligated but the chest was opened,the other groups were the model of myocardial ischemia reperfusion injury.The level of serum creatine phosphokinase(CK) was detected at ischemia 30 min and reperfusion 40 min; The reperfusion injury myocardial malonaldehyole(MDA),superoxide dismutase(SOD),glutathione(GSH),glutathione peroxidase(GSH Px) were detected at reperfusion 40 min.Results:The level of CK was significantly lower in treated groups than in saline group both at ischemia 30 min and reperfusion 40 min;Compared with the pseudooperation group,the MDA was higher and the SOD,GSH and GSH Px were significantly lower in saline group and treated groups;Compared with the saline group,the MDA was higher and the SOD,GSH and GSH Px were significantly lower in treated groups.Conclusion:TMZ can inhibit enzyme leaking from the ischemia reperfusion myocardial cells,and protect the cardiac cells against ischemia reperfusion injury to some extent.The mechanism may be that TMZ can reduce the injury of lipid peroxidation and harmful metabolites to cardiac cell membrane by increasing the content of GSH,the free radical cleaner,and enhancing the activity of SOD and GSH Px.

Objective:To clone the RC-RNase gene and prepare its recombinant prokaryotic construct, and then to express RC-RNase protein using Escherichia coli system. Methods: RC-RNase cDNA was obtained by RT-PCR from liver of Rana catesbeiana, and cloned into pUCm-T plasmid for nucleotide sequencing. Its expression construct was prepared using the 6?His vector pRSET-A, and induced to express by IPTG in Escherichia coli BL21(DE3). Western blotting identified the expression product. Results: A 380 bp long cDNA was obtained from liver of Rana catesbeiana, restriction sites and sequence being consistent to those reported for RC-RNase. After introducing the gene into Escherichia coli and through the induction by IPTG, it was observed a new peptide at the expected position (Mr 16000) on SDS-PAGE gel. This product was proved to be the target protein via Western blotting. It existed in a form of inclusion body and its efficiency reached 12.5% of total bacterial proteins. Conclusion: RC-RNase gene was cloned and expressed in Escherichia coli. The protein could be used for characterizing the biological activities and function of RC-RNase.

Objective:To study the protective effects of trimetazidine (TMZ) on mitochondrial in myocardial ischemia reperfusion rats and its mechanism. Methods: Fifty SD rats were randomly divided into four groups; the pseudooperation group, the saline group and two TMZ treated groups(5 mg/kg and 10 mg/kg). In the pseudooperation group, the coronary artery was not ligated, but the chest was opened. Other groups were subjected to myocardial ischemia reperfusion injury. The serum level of mal onaldehyole ( MDA ) , superoxide dismutase ( SOD ) , glutathione ( GSH ) , glutathione peroxidase (GSH-PX) and the accumulation of Ca2+ in myocardial mitochondrial were detected at the time of 30 min ischemia and 40 min reperfusion. The myocyte ultrastnicture was also observed by electron microscope in the four groups. Results: Compared with the pseudooperation group, the MDA and total Ca2+ were significantly higher and the SOD, GSH, and GSH-PX were significantly lower in saline group and treatment groups. Compared with the saline group, the MDA and total Ca2+ was significantly lower and the SOD, GSH, and GSH-PX were significantly higher in the treatment groups. Conclusion: TMZ could significantly reduce lipid peroxidation in myocardial mitochondrial induced by ischemia and ische-mia-reperfusion. The mechanism may be that TMZ could increase the content of GSH and the acvitity of SOD and GSH-PX, and enhance its antioxidant production. TMZ could protect the cardiac cells by reducing calcium overload in myocardial mitochondrial.

AIM: To isolate peptides targeted binding and internalizing into glioblastoma cell line SWO-38. METHODS: Tumor cells were screened five rounds of whole cell screen through the Ph.D.-12 phage display library. The monoclone specific binding efficiency to the tumor cell was analyzed, and the DNA of phages were extracted, sequenced and translated to the sequences of amino acid. RESULTS: In the phage library after five rounds of screen , 10 of 13 monoclones had highly selective binding to SWO-38 cells. We found two repeated peptide sequences. CONCLUSION: Whole cell screening against tumor cells through random phage peptide library can obtain phage peptides with highly specific binding and internalizing ability. The peptides could be used as a therapy vector for tumor targeted delivery.

Objective To explore the possible effect and mechanism of quercetin (QU) in inhibiting scar formation after the alkali burn of rat's cornea. Methods We established corneal alkali-burn model on right eyes of the SD rats. The rats were divided into five groups randomly. The control group received blank ophthalmic gel; the QU treatment groups received 2.5, 5, 10, or 20g/kg quercetin ophthalmic gel, respectively. The rats were checked by slit-lamp microscope every day for the degree of corneal opacity, then were killed on day 4, 7, 14, 21 and 28 after operation. The infiltration of the inflammatory cells was observed by histology, the arrangement and proliferation of the collagen fibers in the corneal stroma were observed by Masson trichrome staining. The expression of transforming growth factor-β_1 (TGF-β_1) and receptor of transforming growth factor-βⅠ(TGF-βRⅠ) in cornea was observed by immunohistochemical method. Results The corneal opacity was less severe in the QU treatment groups than in the control group (P<0.05). Corneal scar was inhibited better in 10g/kg QU and 20g/kg QU groups than in 2.5g/kg and 5g/kg QU groups, and 10g/kg and 20g/kg QU groups had no significant differences (P>0.05). HE and Masson staining showed that the density of corneal stroma collagen fibers in the QU treatment groups was lower than that in the control group. The expression of TGF-β_1 and TGF-βRⅠ reached the peak on day 7 after alkali burn, and then decreased slowly, which was close to the normal level. The expression of TGF-β_1 and TGF-βRⅠ was inhibited better in 10g/kg and 20g/kg QU groups than in 2.5g/kg and 5g/kg groups, and 10g/kg and 20g/kg QU groups had no significant differences (P>0.05). Conclusion QU ophthalmic gel can reduce formation of corneal scar to a certain extent, 10g/kg is the optimal concentration. QU may play its role by inhibiting the expression of TGF-β1 and TGF-βRⅠ.

Objective:To clarify the contribution of endogenous bFGF, bFGF mRNA and FGFR1 to the abnormal growth and phenotypic transformation of neoplastic tumors cells.Methods:The antisense oligonucleotide primers was used to evaluate the influence of endogenous bFGF on growth of human glioma malignant cell lines SWO-38 in vitro. MTT was used to examine the variety of cells growth treated with bFGF antisense oligonucleotide primers. The methods of ELISA, in situ hybridization, immuno-hischemistry and image analysis were used to detect the expression level of bFGF, bFGF mRNA and FGFR1. The colony formation of cells in soft agar was used to assess the cloning efficiency of the cells after exposed to bFGF antisense oligo-nucleotide primers.Results:The cells multiplication, expression of bFGF mRNA and FGFR1 was inhibited by bFGF antisense oligonucleotide primers,and the cells multiplication was dose-dependent. Treated with antisense oligo-nucleotide primers, the expression of FGFR1 and secretion of bFGF were distinctly reduced, and the inhibition efficiency of cells multiplication of WSO-38 was 48% and the inhibition efficiency of colonies of SWO-38 in soft agar was 35%. The inhibition of cells multiplication can be reversed completely by external bFGF, and the reverse efficiency was 8%.Conclusion:The synthesis of bFGF mRNA and expression of bFGF can be specifically inhibited by antisense oligonucleotide, but the inhibition can be cleared up with the addition of external bFGF. The study suggested that the bFGFantisense oligonucleotide could have good effect in inhibiting of tumor under special condition.