Effect of PDTC on MCP-1 in rejection of cardiac allograft / 中华胸心血管外科杂志

Objective To investigate the effect of pyrrolidine dithiocarbamate(PDTC) on monocyte chemotactic protein1 (MCP-1) in rejection of cardiac allograft and its mechanisms.Methods Heterotopic cervical heart transplantation was performed by cuff-technique.The SD rat recipients were randomly divided into 3 groups:AR group (Acute rejection,n =12),both the recipients and donors were without any treatment.CsA group(n =12),the recipients were treated with 10 mg/kg cyclosporine A after transplantation.PDTC group(n =12),the recipients were treated with 100 mg/kg PDTC after transplantation.All the cardiac allografts were harvested at different time post transplantation according to requirements.We studied allograft myocardial fibrosis wih the help of Masson stain,immuno-histo-chemistry and western blot also were used to detect the expression of MCP-1.Results The survival time of the cardiac allografts was significantly longer in PDTC group than in acute rejection group and CsA group(P ＜ 0.01),and myocardial fibrosis of cardiac allografts in PDTC group was significantly decreased (P ＜ 0.01).The IOD in PDTC group was markedly lower than in CsA group (P ＜ 0.01).Conclusion As the inhibitor of NF-κB,PDTC can significantly relieve rejection of cardiac allograft by inhibiting the expression of MCp-1.

Inhibiting valosin-containing protein suppresses osteosarcoma cell metastasis via AKT/nuclear factor of kappa B signaling pathway in vitro.

Background and Aim: The strategies of targeting valosin-containing protein (VCP) may have therapeutic potential for treating cancer metastasis. In this study, we aim to investigate the correlation of VCP protein expression in osteosarcoma (OS) tissues with pulmonary metastasis and its possible molecular mechanism. Materials and Methods: Expression of VCP in 60 OS specimens was detected by immunohistochemistry (IHC) and the relationship with metastasis was analyzed. An artifi cial micro ribonucleic acid, targeting VCP, was performed to silence the expression of VCP in U2-OS cells. Cell mobility was detected by wound healing and Transwell assays. Western blot and real-time polymerase chain reaction were performed to investigate the expression of VCP in U2-OS cells. Furthermore, the protein of pAKT (phosphorylated serine/threonine protein kinase) and nuclear factor of kappa B protein65 were measured by western blot to evaluate the effect of silencing VCP on AKT/nuclear factor of kappa B (NF-B) signaling pathway. Results: The results showed that the expression level of VCP protein in cases with pulmonary metastases was signifi cantly higher than that in those without metastasis (P = 0.004). The invasion and migration of U2-OS cells were suppressed by silencing VCP. Furthermore, silencing VCP could down-regulate the phosphorylation of AKT and nuclear transfer of NF-B. Conclusions: Our fi ndings suggested that inhibition of VCP could suppress OS cells invasion and migration through down-regulating AKT/NF-B signaling pathway.

Expression and significance of NF-κB and VEGF in the prostatic cancer / 中国综合临床

Objective To explore the relationship between the expression of NF-κB and VEGF and the biological behaviors of prostatic carcinoma.Methods Immunohistochemical method was used to examine the expression of NF-κB and VEGF in 40 cases of benign prostatic hyperplasia (BPH) and 53 cases of prostatic carcinoma.Results The positive rates of NF-κB and VEGF in prostatic carcinoma and BPH were 64.2％ and 69.8％,12.5％ and 37.5％ respectively.There are more cases with positive NF-κB and VEGF expression in prostatic carcinoma group than in the BPH group( x2 =24.976,9.655,P ＜ 0.01 ).The expression of VEGF and NF-κB in prostatic carcinomas increased significantly with the decrease of tumor differentiation and advance of the TNM stages(x2 =15.936,18.459;4.316,14.205,P ＜0.01 or P ＜0.05);The expression of VEGF in prostatic carcinoma was positively correlated with NF-κB ( r =0.297,P =0.027 ).Conclusion The expression of VEGF and NF-κB in prostatic carcinoma are highly correlated with each other and may be suggestive to understand the biological behavior of prostatic carcinoma.

Change of Nuclear Factor-?B Signaling Pathway Alteration in Neonatal Rats with Early Hypoxic-Ischemic Reperfusion Brain Damage / 实用儿科临床杂志

Objective To explore the changes of genes associated with the nuclear factor of kappa B(NF-?B) signaling pathway in neonatal rats with early hypoxic-ischemic reperfusion brain damage(HIRBD).Methods Twenty-four SD rats at age of 7 days,with male to female of 1212,were randomized into normal control group(group A,n=8),hypoxic-ischemia reperfusion for 2 h(group B,n=8) and hypoxic-ischemia reperfusion for 4 h(group C,n=8).The tissues of hippocampus were taken for complete RNA extraction.Gene chip inspection and biological signal analysis technique were used to detect the expression of 113 involved signal molecules of NF-?B pathway.Results Compared with group A,the up-regulated expression was found in Chemokine(C-C motif) ligand 2,Dual specificity phosphatase 1,FBJ osteosarcoma oncogene(Fos) and Toll-like receptor 9.Whereas the expressions of Caspase-1,8,Mitogen-activated protein kinase kinase 6,Mitogen activated protein kinase 3 and Ras homolog gene family member a from Ras-gene famimly was found down-regulated in group B.The up-regulated expression was in Fos,IL-1? and Toll-like receptor 6,but that of down-regulation was found in Caspase-1,Extracellular matrix protein 1,Lysophosphatidic Acid G-protein-coupled receptor 2,Mucosa associated lymphoid tissue lymphoma translocation gene 1,Inhibitor of kappa B kinase epsilon and Ras homolog gene family member c.Conclusions At the early stage of HIRBD,the Toll-like receptors may induce NF-?B activation,leading to the coordinated induction of multiple genes,which is involved in inflammatory,apoptosis and cell proliferation.Genes induced by NF-?B are responsible for the physiopathological process of early brain damage in neonatal rats with HIRBD.

Significance of NF-?B expression in human cerebral tumors / 中国癌症杂志

Purpose:To evaluate the significance of NF ?B P65 protein expression in various human cerebral tumors. Methods:The expression of NF ?B P65 protein in 106 cases of cerebral tumors was studied immunohistochemically. 106 cases included 64 cases of astrocytic tumors and 22 cases of medulloblastoma and 20 cases of meningioma. 10 cases of normal brain tissue were employed as a control group.Results:The positive rate of NF ?B P65 protein of 64 astrocytic tumor specimens was 54.7%; the positive rate of NF ?B P65 protein of 22 cases of medulloblastoma was 36.4% and 5.0% for 20 cases of meningioma. In contrast, none of the normal tissues exhibited NF ?B P65 protein staining. Significant difference were observed between astrocytic tumor group and meningioma, as well as between medulloblastoma and meningioma ( P