目的:探讨慢性牙周炎患者龈沟液中核因子-κB受体活化子配体(receptor activator for NF-κBligand,RANKL)和骨保护素(osteoprotegerin,OPG)的变化及意义。方法:采用滤纸条法收集23例正常对照者和34例慢性牙周炎患者龈沟液(gingival cre...目的:探讨慢性牙周炎患者龈沟液中核因子-κB受体活化子配体(receptor activator for NF-κBligand,RANKL)和骨保护素(osteoprotegerin,OPG)的变化及意义。方法:采用滤纸条法收集23例正常对照者和34例慢性牙周炎患者龈沟液(gingival crevicular fluid,GCF)标本,ELISA法测定上清液RANKL和OPG含量,利用Optimas5.0图像分析软件对检测牙的根尖片进行灰度分析。结果:对照组和慢性牙周炎组临床指标(PD、AL、PLI和SBI)之间存在显著性统计学差异(P<0.01)。2组GCF中RANKL、OPG和RANKL/OPG比值之间存在显著性统计学差异(P<0.01)。慢性牙周炎组GCF中OPG浓度与PD和AL之间存在负相关关系(分别为P<0.01和P<0.05),RANKL浓度及RANKL/OPG比值与根尖片灰度值之间存在负相关关系(P<0.05),GCF中RANKL和OPG浓度及RANKL/OPG比值与PLI和SBI之间无相关关系(P>0.05)。结论:RANKL和OPG在慢性牙周炎患者的牙槽骨组织破坏过程中发挥作用。展开更多
目的:检测内毒素(LPS)刺激后,体外培养人牙龈成纤维细胞(HGFs)表达骨保护素(OPG)和核因子-kB受体活化因子配体(RANKL)的变化,探讨其对牙槽骨吸收的影响。方法:组织块法培养正常HGFs并鉴定来源,以5μg/m l LPS刺激第4代细胞,在0、6、12...目的:检测内毒素(LPS)刺激后,体外培养人牙龈成纤维细胞(HGFs)表达骨保护素(OPG)和核因子-kB受体活化因子配体(RANKL)的变化,探讨其对牙槽骨吸收的影响。方法:组织块法培养正常HGFs并鉴定来源,以5μg/m l LPS刺激第4代细胞,在0、6、12、24、48 h各时间点用免疫细胞化学方法检测OPG和RANKL在细胞中的表达,ELISA法检测相应上清液中OPG的含量并进行统计学分析。结果:免疫细胞化学染色显示正常HGFs表达少量RANKL和OPG,LPS刺激后RANKL的表达未见显著变化,OPG的表达则在刺激后随时间延长而增强,且6、12、24、48 h时间段各实验组均与对照组有显著差异(P<0.01);实验组之间,6、12 h 2时间段有显著差异(P<0.05)。ELISA结果显示培养上清中OPG含量表现同样变化趋势。结论:LPS刺激使体外培养HGFs的OPG表达增强,RANKL无明显变化,可能一定条件下对牙槽骨吸收有抑制作用。展开更多
AIM： To study the effects of hepatitis C virus （HCV） core and non-structural 5A （NS5A） proteins on nuclear factor- k B （NF- k B） activity for understanding their biological function on chronic hepatitis caused ...AIM： To study the effects of hepatitis C virus （HCV） core and non-structural 5A （NS5A） proteins on nuclear factor- k B （NF- k B） activity for understanding their biological function on chronic hepatitis caused by HCV infection. METHODS： Luciferase assay was used to measure the activity of NF-kB in three different cell lines cotransfected with a series of deletion mutants of core protein alone or together with NS5A protein using pNF- k B-Luc as a reporter plasmid. Western blot and indirect immunofluorescence assays were used to confirm the expression of proteins and to detect their subcellular localization, respectively. Furthermore, Western blot was also used to detect the expression levels of NF- k B/p65, NF- k B/p50, and inhibitor k B-a（k B-a）. RESULTS： The wild-type core protein （C191） and its mutant segments （C173 and C158） could activate NF- k B in Huh7 cells only and activation caused by （C191） could be enhanced by NS5A protein. Moreover, the full-length core protein and its different deletion mutants alone or together with NS5A protein did not enhance the expression level of NF- k B. The NF- k B activity was augmented due to the dissociation of NF-k： B-I k： B complex and the degradation of Ik B-a. CONCLUSION：NF- k B is the key transcription factor that can activate many genes that are involved in the cellular immune response and inflammation. Coexpression of the full-length core protein along with NS5A can enhance the NF- k B activation, and this activation may play a significant role in chronic liver diseases including hepatocellular carcinoma associated with HCV infection.展开更多
文摘目的:检测内毒素(LPS)刺激后,体外培养人牙龈成纤维细胞(HGFs)表达骨保护素(OPG)和核因子-kB受体活化因子配体(RANKL)的变化,探讨其对牙槽骨吸收的影响。方法:组织块法培养正常HGFs并鉴定来源,以5μg/m l LPS刺激第4代细胞,在0、6、12、24、48 h各时间点用免疫细胞化学方法检测OPG和RANKL在细胞中的表达,ELISA法检测相应上清液中OPG的含量并进行统计学分析。结果:免疫细胞化学染色显示正常HGFs表达少量RANKL和OPG,LPS刺激后RANKL的表达未见显著变化,OPG的表达则在刺激后随时间延长而增强,且6、12、24、48 h时间段各实验组均与对照组有显著差异(P<0.01);实验组之间,6、12 h 2时间段有显著差异(P<0.05)。ELISA结果显示培养上清中OPG含量表现同样变化趋势。结论:LPS刺激使体外培养HGFs的OPG表达增强,RANKL无明显变化,可能一定条件下对牙槽骨吸收有抑制作用。
基金Supported by the Ph D Program Foundation of Ministry of Education of China, No. 20010486015
文摘AIM： To study the effects of hepatitis C virus （HCV） core and non-structural 5A （NS5A） proteins on nuclear factor- k B （NF- k B） activity for understanding their biological function on chronic hepatitis caused by HCV infection. METHODS： Luciferase assay was used to measure the activity of NF-kB in three different cell lines cotransfected with a series of deletion mutants of core protein alone or together with NS5A protein using pNF- k B-Luc as a reporter plasmid. Western blot and indirect immunofluorescence assays were used to confirm the expression of proteins and to detect their subcellular localization, respectively. Furthermore, Western blot was also used to detect the expression levels of NF- k B/p65, NF- k B/p50, and inhibitor k B-a（k B-a）. RESULTS： The wild-type core protein （C191） and its mutant segments （C173 and C158） could activate NF- k B in Huh7 cells only and activation caused by （C191） could be enhanced by NS5A protein. Moreover, the full-length core protein and its different deletion mutants alone or together with NS5A protein did not enhance the expression level of NF- k B. The NF- k B activity was augmented due to the dissociation of NF-k： B-I k： B complex and the degradation of Ik B-a. CONCLUSION：NF- k B is the key transcription factor that can activate many genes that are involved in the cellular immune response and inflammation. Coexpression of the full-length core protein along with NS5A can enhance the NF- k B activation, and this activation may play a significant role in chronic liver diseases including hepatocellular carcinoma associated with HCV infection.
