Papers by Author: Chun Jing Zhang

Abstract: .Purposes,To explore the effects of carnosine on high glucose-induced apoptosis of human umbilical vein endothelial cells (HUVECs). Methods HUVECs were cultured in vitro. The cellular apoptotic model was made by the addition of high glucose (25 mmol/L), the group of high glucose and carnosine was administered by the addition of high glucose (25 mmol/L) with carnosine (20 mmol/L). In addition, cell apoptosis was detected by the electron microscopy and AnnexinV/PI flow cytometry. Results Compared with the control group, high glucose could induce HUVECs apoptosis under electron microscopy and AnnexinV/PI flow cytometry, while 20 mmol/L carnosine could inhibit the apoptosis induced by high glucose significantly (##P <0.05). Conclusion In this study, carnosine could inhibit high-glucose induced apoptosis of human umbilical vein endothelial cells.

Abstract: To investigate the mechanism underlying the protective effects of glutaredoxin-1 (Grx1) against high glucose-induced apoptosis in umbilical vein endothelial cells. The proliferation of cells was measured by MTT assay. The cells ultra-structure were observed by TEM and the apoptotic rate was detected by the immunofluorescent of Annexin V－FITC/PI with flow cytometer. The level of p-JNK and JNK were evaluated by western bloting. Results showed that Grx1 prevented the inhibitory effect on cell viability induced by high glucose; Grxl could inhibit high glucose-induced apoptosis and restrain apoptosis rate of endothelial cell significantly. The expression level of p-JNK protein significantly increased while that of JNK protein has no insignificantly chang in cells of the high glucose group, After pretreatment with Grx1, the expression level of p-JNK protein decreased. These results demonstrated that Grx1 has protective effects against high glucose-induced apoptosis in HUVECs through inhibition of JNK pathway.

Abstract: There are sufficient evidences that Lewis antigens are tumor-associated molecules and correlated to high grade and poor prognosis tumors. In this study, we investigated the effect of (α1,3)-fucosyltransferase VII overexpression on the synthesis of sLex and adhesive capability of human colon carcinoma HT-29 cells to HUVECs.The pIRES2-EGFP-FucT VII eukaryotic expression vector were transiently transfected into HT-29 cells. The changes of FucT VII protein and mRNA expression were determined by flow cytomet- ry and Real-Time PCR; the effect of FucT VII overexpression on synthesis of its downstream product-sLex is detected by Flow cytometry; Rose-Bengal method is used to assay the capability of HT-29 cell adhesion to HUVECs. Results: Eukaryotic expression vector pIRES2-EGFP-FucT VII was successfully transfected into HT-29 cells and made FucT VII overexpressed; compared with that of control group, expression level of the sLeX on the surface of FucT VII transfected HT-29 cells was significantly higher; FucT VII overexpression could enhance the adhesive capability of HT-29 cells to HUVECs. Our data suggest that overexpression of FucT VII could strengthen adhesion of sLeX-mediated HT-29 cells to HUVECs through upregulating sLeX synthesis.

Abstract: Baicalin has better anti-inflammatory function, antioxidant function and antiviral activity, but the mechanism of the antiinfluenza viral activity of baicalin has not been revealed.Toll-like Receptor 3 and the signal pathways mediated by TLR3 were affected and controlled by the infections with influenza A virus. We report here the significant activity and part mechanism of baicalin against H3N2 influenza A viruses. Baicalin could well protect the damages of cells caused by influenza A virus, it also could effectively inhibit the production of CPE in cells caused by influenza A virus and the inhibition of cells growth. The mechanism of antiinfluenza virus infection of baicalin may be related with the following aspects: to decrease the transcriptional activity of the oxidative stress sensitive transcription factor NF-kappaB and AP-1 by moderately decrease the higher expression level of TLR3 mRNA and the higher expression level of protein; and to further inhibit the mRNA expression of the downstream target genes IL-1β, IL-8, RANTES and IFN-β thereby alleviate the inflammatory injuries and restore the stability and balance of immune function in vivro.

Abstract: Research Teaching is the trend of Higher Education, which will not only help develop undergraduates’ innovative awareness and ability, but also be good for the promotion of teaching and research, cultivation of students’ team spirit, responsibility and dedication. However, there are some issues need our attention and thinking in the implementation of research teaching.

Abstract: To study the underlying mechanism of 20 (S)-Ginsenoside-Rh2 and 20 (R)-Ginsenoside-Rh2 inducing apoptosis of human lung adenocarcinoma A549 cells. In this study, cell death rate and cell survival rate were obtained using typan blue staining cell viability assay, and transmission electron microscopy was used to detect cell apoptosis. Meanwhile, IkappaB phosphorylation expression was analysed by western blotting. Results showed that after A549 cells were treated with 30 μg/mL 20(S)-Rh2 and 20(R)-Rh2 for 48h, cell death rate increased significantly compared with the control group (P<0.05), and nuclear condensation, fragmentation, karyopycnosis and apoptotic bodies were found under transmission electron microscope. There were no significant changes of IkappaB expression after treated with 20(S)-Rh2 and 20(R)-Rh2 (P>0.05). After treated with 20(R)-Rh2, p-IkappaB expression increased obviously between 4h-6h (P<0.05). After treated with 20(S)-Rh2, p-IkappaB expression increased obviously between 1h-2h (P<0.05), back to normal over time after 3h, increased significantly again between 4h-6h (P<0.05), which indicated the activation of IkappaB participated in A549 cell apoptosis induced by Rh2. These results demonstrated that 20(S)-Rh2 and 20(R)-Rh2 both have the functions of activating I-kappaB/NF-kappaB signaling pathway, thus promoting A549 cell apoptosis.