AIM: To investigate the role of nuclear factor κB(NF-κB) in the regulation of Epstein-Barr virus(EBV) latent membrane protein 1(LMP1) in EBV transformed cells. METHODS: LMP1 expression was examined in EBV transforme...AIM: To investigate the role of nuclear factor κB(NF-κB) in the regulation of Epstein-Barr virus(EBV) latent membrane protein 1(LMP1) in EBV transformed cells. METHODS: LMP1 expression was examined in EBV transformed human B lymphocytes with modulation of NF-κB activity. RESULTS: EBV infection is associated with several human cancers. EBV LMP1 is required for efficient transformation of adult primary B cells in vitro, and is expressed in several pathogenic stages of EBVassociated cancers. Regulation of EBV LMP1 involves both viral and cellular factors. LMP1 activates NF-κB signaling pathway that is a part of the EBV transformation program. However, the relation between NF-κB and LMP1 expression is not well established yet. In this report, we found that blocking the NF-κB activity by Inhibitor of κB stimulated LMP1 expression, while the overexpression of NF-κB repressed LMP1 expression in EBV-transformed IB4 cells. In addition, LMP1 repressed its own promoter activities in reporter assays, and the repression was associated with the activation of NF-κB. Moreover, NF-κB alone is sufficient to repress LMP1 promoter activities. CONCLUSION: Our data suggest LMP1 may repress its own expression through NF-κB in EBV transformed cells and shed a light on LMP1 regulation during EBV transformation.展开更多
Objective To investigate the mechanisms of catgut implantation at acupoints on ulcerative colitis. Methods Eighteen SD rats were randomly divided into a normal control group （NC）, a model group （MO） and a catgut i...Objective To investigate the mechanisms of catgut implantation at acupoints on ulcerative colitis. Methods Eighteen SD rats were randomly divided into a normal control group （NC）, a model group （MO） and a catgut implantation group （CI） with 6 rats in each group. Animals in group MO and group CI were treated by trinitro-benzene-sulfonic acid （TNBS） to establish model with colitis. No other treatment was given to the rats in group MO, but catgut was implanted at ＂Shàngjùxū＂ （上 巨虚 ST 37）, ＂Tiānshū＂ （天枢 ST 25） and ＂Dàchángshū＂ （大肠俞 BL 25） in the rats in group CI. The symptoms of diarrhea and bloody stool, and changes in histopathology were detected 15 days after the treatment. Expressions of splenic lymphocyte nuclear factor κB p65（NF-κB p65）and correlated signaling molecules（β2AR）were detected by the western blot method. Results Diarrhea and mucus bloody purulent stool were soon controlled, and mucous injures were obviously improved in group CI. The NF-κB p65 value of splenic lymphocytes was signifi cantly increased （P0.01） and expression of β2AR remarkably reduced in group MO （P0.01）, compared with group NC. But, the NF-κB p65 value was significantly decreased （P0.01） and expression of β2AR remarkably increased in group CI （P 0.01） , compared with group MO. Conclusion Catgut implantation at acupoints is obviously effective in treating experimental colitis. Modulation of NF-κB p65 and the correlated signaling molecules β2AR may be involved in the mechanisms.展开更多
基金Supported by Grants from the NIH CA138213,RR15635Department of Defense W81XWH-12-1-0225(Luwen Zhang)Qianli Wang was partially supported by Undergraduate Creative Activities and Research Experiences and Beckman Scholars Program
文摘AIM: To investigate the role of nuclear factor κB(NF-κB) in the regulation of Epstein-Barr virus(EBV) latent membrane protein 1(LMP1) in EBV transformed cells. METHODS: LMP1 expression was examined in EBV transformed human B lymphocytes with modulation of NF-κB activity. RESULTS: EBV infection is associated with several human cancers. EBV LMP1 is required for efficient transformation of adult primary B cells in vitro, and is expressed in several pathogenic stages of EBVassociated cancers. Regulation of EBV LMP1 involves both viral and cellular factors. LMP1 activates NF-κB signaling pathway that is a part of the EBV transformation program. However, the relation between NF-κB and LMP1 expression is not well established yet. In this report, we found that blocking the NF-κB activity by Inhibitor of κB stimulated LMP1 expression, while the overexpression of NF-κB repressed LMP1 expression in EBV-transformed IB4 cells. In addition, LMP1 repressed its own promoter activities in reporter assays, and the repression was associated with the activation of NF-κB. Moreover, NF-κB alone is sufficient to repress LMP1 promoter activities. CONCLUSION: Our data suggest LMP1 may repress its own expression through NF-κB in EBV transformed cells and shed a light on LMP1 regulation during EBV transformation.
基金Supported by the National Scientific Foundation:30772878
文摘Objective To investigate the mechanisms of catgut implantation at acupoints on ulcerative colitis. Methods Eighteen SD rats were randomly divided into a normal control group （NC）, a model group （MO） and a catgut implantation group （CI） with 6 rats in each group. Animals in group MO and group CI were treated by trinitro-benzene-sulfonic acid （TNBS） to establish model with colitis. No other treatment was given to the rats in group MO, but catgut was implanted at ＂Shàngjùxū＂ （上 巨虚 ST 37）, ＂Tiānshū＂ （天枢 ST 25） and ＂Dàchángshū＂ （大肠俞 BL 25） in the rats in group CI. The symptoms of diarrhea and bloody stool, and changes in histopathology were detected 15 days after the treatment. Expressions of splenic lymphocyte nuclear factor κB p65（NF-κB p65）and correlated signaling molecules（β2AR）were detected by the western blot method. Results Diarrhea and mucus bloody purulent stool were soon controlled, and mucous injures were obviously improved in group CI. The NF-κB p65 value of splenic lymphocytes was signifi cantly increased （P0.01） and expression of β2AR remarkably reduced in group MO （P0.01）, compared with group NC. But, the NF-κB p65 value was significantly decreased （P0.01） and expression of β2AR remarkably increased in group CI （P 0.01） , compared with group MO. Conclusion Catgut implantation at acupoints is obviously effective in treating experimental colitis. Modulation of NF-κB p65 and the correlated signaling molecules β2AR may be involved in the mechanisms.
