目的探讨病原相关模式分子（PAMPs）对抗体诱导的关节炎（CAIA）样小鼠模型建立的影响。方法 7~8周龄Balb/c雌鼠,第0天使用抗体混合物诱导,第3天使用LPS（TLR4激动剂）或Cp G ODN 1826（TLR9激动剂）激发,每天定时观察四肢关节发病情况...目的探讨病原相关模式分子（PAMPs）对抗体诱导的关节炎（CAIA）样小鼠模型建立的影响。方法 7~8周龄Balb/c雌鼠,第0天使用抗体混合物诱导,第3天使用LPS（TLR4激动剂）或Cp G ODN 1826（TLR9激动剂）激发,每天定时观察四肢关节发病情况并进行关节评分;小鼠腹腔注射O111：B4和O55：B5,绘制生存曲线进行毒性分析;ELISA检测PAMPs刺激小鼠巨噬细胞后IL-6、TNF-α的分泌水平;鲎实验定量检测相同浓度下O111：B4和O55：B5的有效活性。结果 PAMPs成功激发CAIA模型炎症,其中O55：B5低死亡率、高成模率;O111：B4的毒性强于O55：B5;O55：B5的炎症因子分泌量显著高于O111：B4和Cp G ODN 1826（P〈0.01）;O111：B4的有效活性显著高于O55：B5（P〈0.01）。结论低毒高致炎性的O55：B5激发模型效果最佳,说明PAMPs能够影响建模效果,而低毒高致炎性PAMPs适合该模型的激发。展开更多
The contents of seven different phenolic acids such as gallic acid, catechinic acid, pyrocatechol, caffeic acid, coumaric acid, ferulic acid and benzoic acid in the poplar leaves （Populus Simonii×Populus Pyramib...The contents of seven different phenolic acids such as gallic acid, catechinic acid, pyrocatechol, caffeic acid, coumaric acid, ferulic acid and benzoic acid in the poplar leaves （Populus Simonii×Populus Pyramibalis c.v and Populus deltoids） suffocated by Methyl jasmonate （MeJA） and Methyl salicylate （MeSA） were monitored for analyzing their functions in interplant communications by using high-pressure liquid chromatography （HPLC）.The results showed that the contents of phenolic acids had obviously difference in leaves exposed to either MeSA or MeJA.When P.deltoides leaves exposed to MeJA or MeSA, the level of gallic acid, coumaric acid, caffeic acid, ferulic acid and benzoic acid was increased, gallic acid in leaves treated with MeJA comes to a peak at 24 h while to a peak at 12-d having leaves treated with MeSA.When P.Simonii ×P.Pyramibalis c.v leaves were exposed to MeJA or MeSA, the level of gallic acid, pyrocatechol and ferulic acid was increased; The catechinic acid and benzoic acid had a little drop; The caffeic acid and coumaric acid were undetected in both suffocated and control leaves.This changed pattern indicated that MeJA and MeSA can act as airborne signals to induce defense response of plants.展开更多
We have previously reported that AD5-10, a novel agonistic monoclonal antibody against DRS, possessed a strong cytotoxic activity in various tumor cells, via induction of caspase-dependent and -independent signaling p...We have previously reported that AD5-10, a novel agonistic monoclonal antibody against DRS, possessed a strong cytotoxic activity in various tumor cells, via induction of caspase-dependent and -independent signaling pathways. The present study further demonstrates that reactive oxygen species （ROS） were generated in abundance in Jurkat leukemia cells upon AD5-10 stimulation and that ROS accumulation subsequently evoked sustained activation of c-Jun N-terminal kinase （JNK）, loss of mitochondrial membrane potential, and release of endonuclease G （Endo G） from mitochondria into the cytosol. The reducing agent, N-acetylcysteine （NAC）, effectively inhibited the sustained activation of JNK, release of Endo G, and cell death in Jurkat cells treated by AD5-10. Moreover, a dominant-negative form of JNK （but not of p38） enhanced NF-κB activation, suppressed caspase-8 recruitment in death-inducing signaling complexes （DISCs）, and reduced adverse effects on mitochondria, thereby inhibiting AD5-10-induced cell death in Jnrkat leukemia cells. These data provide novel information on the DR5-mediated ceil death-signaling path- way and may shed new light on effective strategies for leukemia and solid tumor therapies.展开更多
Objective To assess the prevalence of anti-alpha-enolase antibody in systemic autoimmune diseases in Chinese patients and its role in endothelial cell apoptosis.Methods The reactivity of anti-alpha-enolase antibody in...Objective To assess the prevalence of anti-alpha-enolase antibody in systemic autoimmune diseases in Chinese patients and its role in endothelial cell apoptosis.Methods The reactivity of anti-alpha-enolase antibody in a variety of autoimmune disorders in Chinese patients was evaluated by dot blot assay.Endothelial cell apoptosis was investigated by in vitro incubation of endothelial cells with IgG purified from anti-alpha-enolase antibody-positive sera,with or without pre-incubation with recombinant alpha-enolase.Results Anti-alpha-enolase antibody was prevalent in different systemic autoimmune diseases with relatively high reactivity in Chinese patients.In vitro incubation of endothelial cells with IgG containing anti-alpha-enolase antibody induced apoptosis in a time-and dose-dependent manner.Apoptosis was partly inhibited by pre-incubation of the endothelial cells with recombinant alpha-enolase.Conclusions Our data suggest that alpha-enolase is a common auto-antigen recognized by anti-endothelial cell antibodies in connective tissue disease.Interaction between alpha-enolase and its autoantibody plays a role in endothelial cell apoptosis.Changes other than cell killing may contribute to the pathogenesis of endothelial damage and microvascular lesions.展开更多
文摘目的探讨病原相关模式分子（PAMPs）对抗体诱导的关节炎（CAIA）样小鼠模型建立的影响。方法 7~8周龄Balb/c雌鼠,第0天使用抗体混合物诱导,第3天使用LPS（TLR4激动剂）或Cp G ODN 1826（TLR9激动剂）激发,每天定时观察四肢关节发病情况并进行关节评分;小鼠腹腔注射O111：B4和O55：B5,绘制生存曲线进行毒性分析;ELISA检测PAMPs刺激小鼠巨噬细胞后IL-6、TNF-α的分泌水平;鲎实验定量检测相同浓度下O111：B4和O55：B5的有效活性。结果 PAMPs成功激发CAIA模型炎症,其中O55：B5低死亡率、高成模率;O111：B4的毒性强于O55：B5;O55：B5的炎症因子分泌量显著高于O111：B4和Cp G ODN 1826（P〈0.01）;O111：B4的有效活性显著高于O55：B5（P〈0.01）。结论低毒高致炎性的O55：B5激发模型效果最佳,说明PAMPs能够影响建模效果,而低毒高致炎性PAMPs适合该模型的激发。
基金This research is supported by National Natural Science Foundation of China (No.30170764)
文摘The contents of seven different phenolic acids such as gallic acid, catechinic acid, pyrocatechol, caffeic acid, coumaric acid, ferulic acid and benzoic acid in the poplar leaves （Populus Simonii×Populus Pyramibalis c.v and Populus deltoids） suffocated by Methyl jasmonate （MeJA） and Methyl salicylate （MeSA） were monitored for analyzing their functions in interplant communications by using high-pressure liquid chromatography （HPLC）.The results showed that the contents of phenolic acids had obviously difference in leaves exposed to either MeSA or MeJA.When P.deltoides leaves exposed to MeJA or MeSA, the level of gallic acid, coumaric acid, caffeic acid, ferulic acid and benzoic acid was increased, gallic acid in leaves treated with MeJA comes to a peak at 24 h while to a peak at 12-d having leaves treated with MeSA.When P.Simonii ×P.Pyramibalis c.v leaves were exposed to MeJA or MeSA, the level of gallic acid, pyrocatechol and ferulic acid was increased; The catechinic acid and benzoic acid had a little drop; The caffeic acid and coumaric acid were undetected in both suffocated and control leaves.This changed pattern indicated that MeJA and MeSA can act as airborne signals to induce defense response of plants.
基金Acknowledgments We thank Dr Shimin Hu for his generous gifts of constructs. This work was partially supported by National Natural Science Foundation of China （Grant Nos. 30571687 and 30721063） and by State Key Basic Research Program of China （Grant No. 2007CB507404）.
文摘We have previously reported that AD5-10, a novel agonistic monoclonal antibody against DRS, possessed a strong cytotoxic activity in various tumor cells, via induction of caspase-dependent and -independent signaling pathways. The present study further demonstrates that reactive oxygen species （ROS） were generated in abundance in Jurkat leukemia cells upon AD5-10 stimulation and that ROS accumulation subsequently evoked sustained activation of c-Jun N-terminal kinase （JNK）, loss of mitochondrial membrane potential, and release of endonuclease G （Endo G） from mitochondria into the cytosol. The reducing agent, N-acetylcysteine （NAC）, effectively inhibited the sustained activation of JNK, release of Endo G, and cell death in Jurkat cells treated by AD5-10. Moreover, a dominant-negative form of JNK （but not of p38） enhanced NF-κB activation, suppressed caspase-8 recruitment in death-inducing signaling complexes （DISCs）, and reduced adverse effects on mitochondria, thereby inhibiting AD5-10-induced cell death in Jnrkat leukemia cells. These data provide novel information on the DR5-mediated ceil death-signaling path- way and may shed new light on effective strategies for leukemia and solid tumor therapies.
基金Supported by National Natural Science Foundation of China (30400411)
文摘Objective To assess the prevalence of anti-alpha-enolase antibody in systemic autoimmune diseases in Chinese patients and its role in endothelial cell apoptosis.Methods The reactivity of anti-alpha-enolase antibody in a variety of autoimmune disorders in Chinese patients was evaluated by dot blot assay.Endothelial cell apoptosis was investigated by in vitro incubation of endothelial cells with IgG purified from anti-alpha-enolase antibody-positive sera,with or without pre-incubation with recombinant alpha-enolase.Results Anti-alpha-enolase antibody was prevalent in different systemic autoimmune diseases with relatively high reactivity in Chinese patients.In vitro incubation of endothelial cells with IgG containing anti-alpha-enolase antibody induced apoptosis in a time-and dose-dependent manner.Apoptosis was partly inhibited by pre-incubation of the endothelial cells with recombinant alpha-enolase.Conclusions Our data suggest that alpha-enolase is a common auto-antigen recognized by anti-endothelial cell antibodies in connective tissue disease.Interaction between alpha-enolase and its autoantibody plays a role in endothelial cell apoptosis.Changes other than cell killing may contribute to the pathogenesis of endothelial damage and microvascular lesions.
