目的:探讨抗白细胞介素-6(IL-6)单克隆抗体司妥昔单抗(siltuximab)对IL-6介导的基因表达的影响。方法:采用Affymetrix人类基因组表达谱芯片U133 Plus 2.0,检测经IL-6处理的卵巢癌细胞株SKOV-3(SKOV-3+IL-6)和Caov-3(Caov-3+IL-6)中相关...目的:探讨抗白细胞介素-6(IL-6)单克隆抗体司妥昔单抗(siltuximab)对IL-6介导的基因表达的影响。方法:采用Affymetrix人类基因组表达谱芯片U133 Plus 2.0,检测经IL-6处理的卵巢癌细胞株SKOV-3(SKOV-3+IL-6)和Caov-3(Caov-3+IL-6)中相关基因的表达水平。通过Taq Man实时定量PCR分析,研究siltuximab对卵巢癌细胞株(SKOV-3、Caov-3)中IL-6介导的基因表达的影响。结果:1经Affymetrix人类基因组测定:经IL-6处理后,SKOV-3+IL-6和Caov-3+IL-6细胞株中分别有506个和674个基因上调,其中27个基因在两种细胞株中均表现出10倍上调。2经siltuximab处理后,在SKOV-3+IL-6+siltuximab和Caov-3+IL-6+siltuximab细胞株中,分别有634个和679个基因出现10倍降调,还有31个基因在两种细胞中均表现出10倍降调。3对在两种细胞株中经IL-6处理后均过度表达的多肽三烯B4(UGT2B4)和ATP细胞膜钙转运2(ATP2B2)基因经siltuximab处理后,Taq Man实时定量PCR示,SKOV-3+IL-6+siltuximab和Caov-3+IL-6+siltuximab细胞株中UGT2B4基因的表达分别降调3倍和17倍,ATP2B2基因的表达分别降调10倍和7倍。结论:IL-6在卵巢癌发生发展中发挥着一定作用,是治疗卵巢癌的一个重要的靶点。siltuximab可以有效地阻断IL-6介导的UGT2B4和ATP2B2基因在这些细胞中的表达,可能为卵巢癌的基因治疗提供新思路。展开更多
Currently clinicians all around the world are experiencing a pandemic caused by severe acute respiratory syndrome coronavirus 2(SARS-CoV-2).The clinical presentation of this pathology includes fever,dry cough,fatigue ...Currently clinicians all around the world are experiencing a pandemic caused by severe acute respiratory syndrome coronavirus 2(SARS-CoV-2).The clinical presentation of this pathology includes fever,dry cough,fatigue and acute respiratory distress syndrome that can lead to death infected patients.Current studies on coronavirus disease 2019(COVID-19)continue to highlight the urgent need for an effective therapy.Numerous therapeutic strategies have been used until now but,to date,there is no specific effective treatment for SARS-CoV-2 infection.Elevated inflammatory cytokines have been reported in patients with COVID-19.Evidence suggests that elevated cytokine levels,reflecting a hyperinflammatory response secondary to SARS-CoV-2 infection,are responsible for multi-organ damage in patients with COVID-19.For these reason,numerous randomized clinical trials are currently underway to explore the effectiveness of biopharmaceutical drugs,such as,interleukin-1 blockers,interleukin-6 inhibitors,Janus kinase inhibitors,in COVID-19.The aim of the present paper is to briefly summarize the pathogenetic rationale and the state of the art of therapeutic strategy blocking hyperinflammation.展开更多
文摘目的:探讨抗白细胞介素-6(IL-6)单克隆抗体司妥昔单抗(siltuximab)对IL-6介导的基因表达的影响。方法:采用Affymetrix人类基因组表达谱芯片U133 Plus 2.0,检测经IL-6处理的卵巢癌细胞株SKOV-3(SKOV-3+IL-6)和Caov-3(Caov-3+IL-6)中相关基因的表达水平。通过Taq Man实时定量PCR分析,研究siltuximab对卵巢癌细胞株(SKOV-3、Caov-3)中IL-6介导的基因表达的影响。结果:1经Affymetrix人类基因组测定:经IL-6处理后,SKOV-3+IL-6和Caov-3+IL-6细胞株中分别有506个和674个基因上调,其中27个基因在两种细胞株中均表现出10倍上调。2经siltuximab处理后,在SKOV-3+IL-6+siltuximab和Caov-3+IL-6+siltuximab细胞株中,分别有634个和679个基因出现10倍降调,还有31个基因在两种细胞中均表现出10倍降调。3对在两种细胞株中经IL-6处理后均过度表达的多肽三烯B4(UGT2B4)和ATP细胞膜钙转运2(ATP2B2)基因经siltuximab处理后,Taq Man实时定量PCR示,SKOV-3+IL-6+siltuximab和Caov-3+IL-6+siltuximab细胞株中UGT2B4基因的表达分别降调3倍和17倍,ATP2B2基因的表达分别降调10倍和7倍。结论:IL-6在卵巢癌发生发展中发挥着一定作用,是治疗卵巢癌的一个重要的靶点。siltuximab可以有效地阻断IL-6介导的UGT2B4和ATP2B2基因在这些细胞中的表达,可能为卵巢癌的基因治疗提供新思路。
文摘Currently clinicians all around the world are experiencing a pandemic caused by severe acute respiratory syndrome coronavirus 2(SARS-CoV-2).The clinical presentation of this pathology includes fever,dry cough,fatigue and acute respiratory distress syndrome that can lead to death infected patients.Current studies on coronavirus disease 2019(COVID-19)continue to highlight the urgent need for an effective therapy.Numerous therapeutic strategies have been used until now but,to date,there is no specific effective treatment for SARS-CoV-2 infection.Elevated inflammatory cytokines have been reported in patients with COVID-19.Evidence suggests that elevated cytokine levels,reflecting a hyperinflammatory response secondary to SARS-CoV-2 infection,are responsible for multi-organ damage in patients with COVID-19.For these reason,numerous randomized clinical trials are currently underway to explore the effectiveness of biopharmaceutical drugs,such as,interleukin-1 blockers,interleukin-6 inhibitors,Janus kinase inhibitors,in COVID-19.The aim of the present paper is to briefly summarize the pathogenetic rationale and the state of the art of therapeutic strategy blocking hyperinflammation.
