Both thymocytes and tumor cells express M2 type isoenzyme of pyruvate kinase(M2PK),which is different from R type isoenzyme of pyruvate kinase(RPK)that is expressed in erythrocytes.In this report,the effect of RPK and...Both thymocytes and tumor cells express M2 type isoenzyme of pyruvate kinase(M2PK),which is different from R type isoenzyme of pyruvate kinase(RPK)that is expressed in erythrocytes.In this report,the effect of RPK and M2PK on the transcription of human immunodeficiency virus type 1(HIV-1)was tested.The results indicated that M2PK could enhance HIV-1 transcription from its long terminal repeat(LTR)promoter,while RPK did not have such an effect.Specific down-regulation of M2PK could inhibit HIV-1 transcription from its LTR region.Furthermore,it was found that the C terminal region of M2PK is responsible for this effect.Collectively,the cellular factor M2PK that is expressed in thymocytes could facilitate the transcription of HIV-1.展开更多
Catalpol is the main active ingredient of an extract from Radix rehmanniae,which in a previous study showed a protective effect against various types of tissue injury.However,a protective effect of catalpol on uterine...Catalpol is the main active ingredient of an extract from Radix rehmanniae,which in a previous study showed a protective effect against various types of tissue injury.However,a protective effect of catalpol on uterine inflammation has not been reported.In this study,to investigate the protective mechanism of catalpol on lipopolysaccharide(LPS)-induced bovine endometrial epithelial cells(bEECs)and mouse endometritis,in vitro and in vivo inflammation models were established.The Toll-like receptor 4(TLR4)/nuclear factor-κB(NF-κB)signaling pathway and its downstream inflammatory factors were detected by enzyme-linked immunosorbent assay(ELISA),quantitative real-time polymerase chain reaction(qRT-PCR),western blot(WB),and immunofluorescence techniques.The results from ELISA and qRT-PCR showed that catalpol dose-dependently reduced the expression of pro-inflammatory cytokines such as tumor necrosis factorα(TNF-α),interleukin(IL)-1β,and IL-6,and chemokines such as C-X-C motif chemokine ligand 8(CXCL8)and CXCL5,both in bEECs and in uterine tissue.From the experimental results of WB,qRT-PCR,and immunofluorescence,the expression of TLR4 and the phosphorylation of NF-κB p65 were markedly inhibited by catalpol compared with the LPS group.The inflammatory damage to the mouse uterus caused by LPS was greatly reduced and was accompanied by a decline in myeloperoxidase(MPO)activity.The results of this study suggest that catalpol can exert an anti-inflammatory impact on LPS-induced bEECs and mouse endometritis by inhibiting inflammation and activation of the TLR4/NF-κB signaling pathway.展开更多
目的：观察芍药汤对湿热型溃疡性结肠炎（ulcerative colitis,UC）大鼠模型结肠组织中高迁移率族蛋白B1（high mobility group protein B1,HMGB1）的调控,分析其对衔接蛋白髓样分化因子88（My D88）和核转录因子-κB（NF-κB）的影响,...目的：观察芍药汤对湿热型溃疡性结肠炎（ulcerative colitis,UC）大鼠模型结肠组织中高迁移率族蛋白B1（high mobility group protein B1,HMGB1）的调控,分析其对衔接蛋白髓样分化因子88（My D88）和核转录因子-κB（NF-κB）的影响,探讨芍药汤对湿热型UC的作用机制。方法：Wistar大鼠雌雄各60只,分为空白组、模型组、芍药汤高、中、低剂量组、柳氮磺砒啶组,以2,4,6-三硝基苯磺酸（TNBS）结合乙醇复合法复制湿热型UC大鼠模型,芍药汤高、中、低剂量灌胃,柳氮磺砒啶组予柳氮磺砒啶研磨成粉配置成与中药等体积液体灌胃,空白组及模型组予等体积生理盐水灌胃,连续21 d。取结肠组织,运用实时荧光定量聚合酶链式反应（Real-time,PCR）法、蛋白免疫印迹法（Western blot）检测mRNA及蛋白表达,苏伊红-木精（HE）染色观察病理切片。结果：与空白组比较,模型组HMGB1,My D88,NF-κB蛋白及mRNA表达明显升高（P〈0.05）;与模型组比较,芍药汤各组、柳氮磺砒啶组HMGB1,My D88,NF-κB蛋白及mRNA表达均有不同程度地下降,芍药汤高剂量组及柳氮磺砒啶组最为显著（P〈0.05）。结论：芍药汤可调控HMGB1抑制TLRs信号通路中My D88,NF-κB基因表达,减弱湿热型UC的炎症反应。展开更多
基金This work was supported by the National Basic Research Program of China(973 Program)(No.2006CB504305)National Special Research Program of Major Infectious Diseases(No.2008ZX10001-002)the 111 Project(No.B06018).
文摘Both thymocytes and tumor cells express M2 type isoenzyme of pyruvate kinase(M2PK),which is different from R type isoenzyme of pyruvate kinase(RPK)that is expressed in erythrocytes.In this report,the effect of RPK and M2PK on the transcription of human immunodeficiency virus type 1(HIV-1)was tested.The results indicated that M2PK could enhance HIV-1 transcription from its long terminal repeat(LTR)promoter,while RPK did not have such an effect.Specific down-regulation of M2PK could inhibit HIV-1 transcription from its LTR region.Furthermore,it was found that the C terminal region of M2PK is responsible for this effect.Collectively,the cellular factor M2PK that is expressed in thymocytes could facilitate the transcription of HIV-1.
基金Project supported by the National Natural Science Foundation of China(No.31472254)
文摘Catalpol is the main active ingredient of an extract from Radix rehmanniae,which in a previous study showed a protective effect against various types of tissue injury.However,a protective effect of catalpol on uterine inflammation has not been reported.In this study,to investigate the protective mechanism of catalpol on lipopolysaccharide(LPS)-induced bovine endometrial epithelial cells(bEECs)and mouse endometritis,in vitro and in vivo inflammation models were established.The Toll-like receptor 4(TLR4)/nuclear factor-κB(NF-κB)signaling pathway and its downstream inflammatory factors were detected by enzyme-linked immunosorbent assay(ELISA),quantitative real-time polymerase chain reaction(qRT-PCR),western blot(WB),and immunofluorescence techniques.The results from ELISA and qRT-PCR showed that catalpol dose-dependently reduced the expression of pro-inflammatory cytokines such as tumor necrosis factorα(TNF-α),interleukin(IL)-1β,and IL-6,and chemokines such as C-X-C motif chemokine ligand 8(CXCL8)and CXCL5,both in bEECs and in uterine tissue.From the experimental results of WB,qRT-PCR,and immunofluorescence,the expression of TLR4 and the phosphorylation of NF-κB p65 were markedly inhibited by catalpol compared with the LPS group.The inflammatory damage to the mouse uterus caused by LPS was greatly reduced and was accompanied by a decline in myeloperoxidase(MPO)activity.The results of this study suggest that catalpol can exert an anti-inflammatory impact on LPS-induced bEECs and mouse endometritis by inhibiting inflammation and activation of the TLR4/NF-κB signaling pathway.
