Objective To study the effects of nitric oxide (NO) synthesis on serum interleukin 1? (IL-1?) and tumor necrosis factor ? (TNF-?) levels in liver ischemic preconditioning (IP) in rats. Methods 169 rats were randomly divided into ischemia/reperfusion (I/R) group, IP group,L-arginine plus IP (L-Arg+IP) group and sham operation group (S group). The concentrations of plasma NO, serum IL-1? and TNF-? were measured at 2h, 24h and 1 week after models were set up. Results ⑴ Plasma NO concentrations: In group IP and group L-Arg+IP,the NO concentration at all the 3 time points were significantly higher than those in group S (P0 05). Conclusions Liver ischemic preconditioning could down-regulate the levels of blood IL-1? and TNF-?, which may relate to the increase of NO synthesis. The increase of NO synthesis could enlarge this down-regulation effect, and further enhance the protective effect of IP on the liver I/R injury.

Objective To investigate the effect of herpes simplex virus thymidine kinase/ganciclovir (HSV-TK/GGV)system driven by human alpha fetoprotein(AFP)enhancer on hepatocellular carcinoma(HCC)cells in vitro and in vivo.Methods HCC-specific eukarotypic expression vector carrying suicide gene driven by AFP enhancer(pAFP-cDNA3.1-TK)was constructed.The plasmid was trasfected to AFP-positive HepG2 cells and AFP-negative SMMC7721 cells by liposomes.Protein and mRNA expressions of TK were detected by RT-PCR or Western blot.The survival rates of HCC cells were detected by methyl thiazolyl tetrazolium assay.The effects of GGV on the in vitro proliferation,survival and apoptosis of HCC cells were observed,and the inhibitive effect of GGV on the survival of HCC cells in vivo was also detected.All data were analyzed by using the t test.Results The pAFP-cDNA3.1-TK was successfully constructed and transfected to the HCC cells.The protein and mRNA expressions of TK were detected in AFP-positive HepG2 cells.GGV dose-and time-dependently inhibited the growth and induced the apoptosis of HepG2 cells in vitro,but it had no effect on SMMC7721 cells.No protein or mRNA expression of TK was detected in the SMMC7721 cells.There was a significant difference on the inhibitory effects of GGV on HepG2 cells and SMMC7721 cells(t =2.58,2.73,3.12,P ＜0.05).GGV specifically inhibited the growth of AFP-positive HepG2 cells,and the inhibition rate was 46%;the growth of AFP-negative SMMC7721 cells was not influenced by GGV.There was a significant difference in the inhibitive effect of GGV on the growth of HepG2 cells and SMMC7721 cells(t = 3.36,P ＜ 0.05).Conclusion HSV-TK/GGV systemdriven by human APF enhancer kills APF-positive HCC cells and inhibits the growth of HCC cells.

Objective To study the early prediction of infection in acute pancreatitis in rats by plasma procalcitonin (PCT) and c-reactive (CRP) detection.Methods Eighty SD rats were randomly assigned into acute infected pancreatitis group (I, n=20), pancreatitis control group (C, n=40) and sham-operated group (S, n=20). Blood samples were collected pre- (0h) and post-operatively (12h, 24h and 48h). Plasma CRP was analyzed by ELISA. Plasma and liver PCT was detected by Western blot.Results (1). Ascitic infection occurred in all the group B rats and 16 of 40 rats of group C (analyzed as group C1), and did not occur in the other 20 of 40 rats of group C (analyzed as group C2) and group S. (2). The plasma CRP concentrations elevated gradually after the model setup in group B and C1, which were significantly higher at 48h than those in group C2 and group S. (3). PCT was detected in high levels in plasma and liver tissues in group B and C1 at 48h post-operatively, and they were sighificantly higher than those in group C2 and group S.Conclusions PCT can predict early infection of acute pancreatitis, and detection of PCT combined with plasma CRP may help in the differentiation of acute infected pancreatitis. The liver may be an important organ for synthesis of PCT.

ObjectiveTo study the value of C-reactive protein (CRP) and interleukin-6(IL-6) in the (diagnosis) of acute pancreatitis (AP) associated with infection. MethodsSixty SD rats were randomly (assigned) into group AP (n=40) and sham-operation group (S, n=20). Plasma CRP and IL-6 were detected before AP(0h), and at 12h, 24h and 48h after AP. Serum amylase detection and ascitic bacteria culture were carried out at 48h. Results(1)In AP group, 36 rats were alive. Ascitic infection developed in 16 cases (group AP1), and not in the other 20 cases (group AP2). (2)Plasma CRP and IL-6 levels in group AP1 and AP2 were significantly higher than those in group S (all, P0.05). (3)In group AP1, IL-6 and CRP elevated significantly at all time periods after the model setup (P0.05). (Conclusions)Plasma CRP has predictive value in the diagnosis of early infection in acute pancreatitis, but plasma IL-6 is not sensitive to secondary bacteria infection in acute pancreatitis.

Objective To study the protective effect of liver ischemic preconditioning on the extrahepatic organs injury induced by liver ischemia/repurfusion in rats. Methods Seventy-two Sprague-Dawley rats were randomly assigned into group IP,group I/R and group S (sham-operation group), each group had 24 rats. After ischemic preconditioning and ischemia/repurfusion animal models were set up,the pathological changes of small intestine, pancreas, myocardium, kidney, lung, brain and skeletal muscle tissues were observed at 2h,24h and 1week,respealively. Results (1) The degree(s) of small intestinal injury: at 2h and 24h, The injury in group IP and group I/R were significantly higher than that in group S (all P

Objective To study the role of nitiric oxide (NO) in the liver ischemic precondition (IP) in rats. Methods 131 rats were randomly assigned to ischemia/reperfusion (I/R)group, IP group and sham-operation(S) group. The plasma NO, alanine aminotransferase (ALT) and aspartate aminotransferase (AST), the pathological change of liver and rat mortality were observed at 2 hours, 24 hours and 1 week after operation. Results (1) The plasma NO level grew soon after operation in group IP, and was significantly higher than that in group S in all three time points (P0.05), and higher at 1 week (P

ObjectiveTo investigate the feasibility and isolation efficiency of percutaneous selective isolated hepatic perfusion chemotherapy(PSIHP). MethodsSix pigs underwent the procedure of routine transhepatic arterial infusion(HAI) and 6 underwent PSIHP.5-FU was used in this study. The drug(5-FU) (concentration) of blood from hepatic and systemic veins of both groups was observed. Liver tissue was (investigated) for pathologic changes. ResultsThe peak level of 5-FU concentration in blood from right (hepatic) vein and systemic vein in HAI group was(4082.530415.213)mg/L and (1682.230216.834)mg/L respectively.In PSIHP group, the peak level(5-FU) was(5321.711517.318)mg/L and(510.83452.518)mg/L, respectively.There was a statistically significant difference between HAI group an PSIHP group(P

To study the therapeutic effects of herpes simplex virus thymidine kinase (HSV-TK) gene transferred by the EBV-based expression vector (pDR2) on experimental hepatocellular carcinoma, pDR2-TK gene was delivered into human hepatocellular carcinoma cell line SMMC-7721 by using liposome-mediated transfection technique，and then gene expression was detected by RT-PCR, and the killing effects were examined through MTT method. In the nude mice hepatoma model，the antitumor effects of pDR2-TK /GCV system was evaluated in terms of tumor growth. MTT results showed that the pDR2-TK /GCV had cytotoxic effect and about 70 % SMMC-7721 cells were killed when GCV was at 1000 μmol/L. In vivo experiment showed that the tumor size in nude mice with transferred pDR2-TK gene was significantly smaller than that in control group (P<0.01). On the 10th day the tumor in 3 mice (60 %） disappeared completely after GCV treatment. It is concluded that the pDR2-TK/GCV system has marked killing effects on the experimental hepatocellular carcinoma.

BACKGROUND:There are many postmenopausal women taking hormone, which leads to much loss of bone mass, further inducing fragility fractures. The studies on the hormone exposure combined with ovariectomy-induced osteoporotic model are still immature, and the related molecular mechanism remains unclear. OBJECTIVE: To establish the rat osteoporotic model induced by ovariectomy combined with glucocorticoid exposure and to explore the underlying molecular mechanism. METHODS: Thirty 3-month-old female Sprague-Dawley rats were randomly divided into blank control, sham and model groups (n=10 per group). The rats in the blank control group received no intervention; rats in the sham group were clipped off a little of coeliac adipose tissue; the model rats received bilateral ovariectomy and 4-week administration of glucocorticoid. RESULTS AND CONCLUSION:At 4 weeks after modeling, compared with blank control and sham groups, the model group showed significantly lower bone mineral density of the femur, number of bone trabeculae and bone volume/total volume, and significantly wider bone trabecular spacing. Additionally, the model group revealed the damaged bone trabecular structure and thiner cortical bone. The expression level of Runx2 was downregulated whereas both collagen type 1α1 and peroxisome proliferators activated receptor γ mRNA were upregulated in the model group. These findings suggest that ovariectomized rats exposed to glucocorticoid rapidly develop femur osteoporosis, maybe by downregulating the expression of Runx2, as well as upregualting collagen type 1α1 and peroxisome proliferators activatedreceptor γ mRNA.

To study the therapeutic effects of herpes simplex virus thymidine kinase (HSV-TK) gene transferred by the EBV-based expression vector (pDR2) on experimental hepatocellular carcinoma, pDR2-TK gene was delivered into human hepatocellular carcinoma cell line SMMC-7721 by using liposome-mediated transfection technique，and then gene expression was detected by RT-PCR, and the killing effects were examined through MTT method. In the nude mice hepatoma model，the antitumor effects of pDR2-TK /GCV system was evaluated in terms of tumor growth. MTT results showed that the pDR2-TK /GCV had cytotoxic effect and about 70 % SMMC-7721 cells were killed when GCV was at 1000 μmol/L. In vivo experiment showed that the tumor size in nude mice with transferred pDR2-TK gene was significantly smaller than that in control group (P<0.01). On the 10th day the tumor in 3 mice (60 %） disappeared completely after GCV treatment. It is concluded that the pDR2-TK/GCV system has marked killing effects on the experimental hepatocellular carcinoma.