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 To investigate the effects of PD98059, the specific blocking agent of mitogen extracellular signal responsive kinase, on the cell cycle, cell proliferation, type Ⅰ collagen's secretion and transforming growth factor(TGF)? 1mRNA expression of rat hepatic stellate cells (HSC) stimulated by acetaldehyde. Methods Rat HSC stimulated by acetaldehyde were incubated with different concentration of PD98059. Cell cycle was analysed by flow cytometry. Cell proliferation was assessed by MTT colorimetric assay. Type Ⅰcollagen of culture medium was detected by enzyme linked immunoadsordent assay (ELISA). TGF? 1mRNA expression were examined by RT PCR. Results 20,50,100 ?mol/L PD98059 could significantly inhibit proliferation and induced G0/G1 phase arrest of HSC stimulated by acetaldehyde in a does dependent manner. 50,100 ?mol/L PD98059 could markedly inhibit type Ⅰcollagen's secretion and TGF? 1mRNA expression of HSC stimulated by acetaldehyde. Conclusion The extracellular signal regulated kinase signal transduction passway regulates the cell proliferation, type Ⅰcollagen's secretion and TGF? 1mRNA expression of rat HSC stimulated by acetaldehyde,which might be partly related to its regulative effect on the cell cycle.

Objective To investigate the expression and clinical significance of serum PTX3 in HCC patients. Methods We selected 78 HCC patients as the liver cancer group, and 78 cases of healthy subjects as the healthy control group. The PTX3 levels were detected and compared between the two groups. The differences of PTX3 levels in patients with different pathological characteristics were analyzed. ROC curve was used to analyze the auxiliary diagnostic value of serum PTX3 in HCC. Results PTX3 level in HCC patients was higher than that in healthy control group (P < 0.05). PTX3 level in stage Ⅰ group was higher than those in the stage Ⅱ group and Ⅲ group (P < 0.05). PTX3 level in patients with tumor ≥5cm was significantly lower than that with tumor diameter < 5cm (P < 0.05). In addition, PTX3 level in patients with HBV infection was significantly higher than that without HBV infection (P < 0.05). The AUC was 0.938. Conclusion The serum PTX3 level is significantly increased in patients with HCC. It has auxiliary diagnostic value for HCC.

OBJECTIVE: To determine the effect and molecular mechanism of DNA damage caused by suicide gene therapy system HSV-TK/GCV under Tet-On regulation in human breast cancer cell line MCF-7 infected by recombinant adeno-associated virus (rAAV). METHODS: We used comet assay to detect the effect of HSV-TK/GCV suicide gene regulation system on MCF-7 DNA damage, and analyzed the expression change of relative DNA damage response active genes and proteins with RT-PCR and Western blot. RESULTS: Compared with other control groups, the comet assay showed that MCF-7 cells with HSV-TK/GCV treatment had obvious comet tails, and the expression level of DNA damage response active genes and proteins changed obviously in the HSV-TK/GCV treatment group,such as ATM, p53 and p27,but CyclinE and CDK2 did not change. CONCLUSION DNA damage on MCF-7 cells is resulted from HSV-TK/GCV in suicide gene therapy system through a p53-dependent signal pathway, causing cell cycle arrest and cell death.
Breast Neoplasms ; genetics ; pathology ; therapy ; DNA Damage ; Dependovirus ; genetics ; Female ; Ganciclovir ; metabolism ; pharmacology ; Gene Expression Regulation, Neoplastic ; Genes, Transgenic, Suicide ; genetics ; Genetic Therapy ; Humans ; MCF-7 Cells ; Recombinant Fusion Proteins ; genetics ; metabolism ; Simplexvirus ; enzymology ; Thymidine Kinase ; genetics