As a main pro-inflammatory factor, the up-regulation of TNF-α in RA patients plays a pivotal role in RA pathogenesis. The process of TNF production starts with the binding of a ligand( which is commonly a microbial p...As a main pro-inflammatory factor, the up-regulation of TNF-α in RA patients plays a pivotal role in RA pathogenesis. The process of TNF production starts with the binding of a ligand( which is commonly a microbial product) to a cell surface Toll receptor, which stimulates a signal transduction pathway that activates NF - κB transcription factors. Activated NF - κB enters nuclei and induces the transcription of genes associated with inflammation, including those coding for TNF. The production of TNF and other inflammatory cytokines serves to recruit other inflammatory cells, which in turn release cytokines and subsequently amplify the immune response. TNF exerts its effect via binding of TNFRland TNFR2 receptors. Many experimental and clinical study have proved the effectiveness of TNF - αa ctivity blockade. Recent therapeutic interventions, including TNF - α and IL - 1 inhibitors, strongly support the importance of cytokines in RA. The mechanism of anti - TNF - α action in vivo is complex and probably includes suppression of other pro - inflammatory cytokines, decreased synovial cellular infiltration, interference with osteoclast activation, and decreased angiogenisis. Studies using anti -TNF agents clearly show that they can slow or prevent the progression of bone and cartilage damage in RA. This activity probably involves suppression of osteoclasts in joint lesions. Etanereept, Infliximab and adalimumab are the three main biologic agents that were fo-cused on clinically at present.展开更多
为了研究治伤巴布剂对大鼠早期骨折愈合及对肿瘤坏死因子-α(tumornecrosisfactor-α,TNF-α)表达的影响,将45只SPF级雄性大鼠随机分为空白组、模型组、治伤巴布剂组3个组,每组15只。空白组不造模,其余2组予以闭合造模,造模成功后治伤...为了研究治伤巴布剂对大鼠早期骨折愈合及对肿瘤坏死因子-α(tumornecrosisfactor-α,TNF-α)表达的影响,将45只SPF级雄性大鼠随机分为空白组、模型组、治伤巴布剂组3个组,每组15只。空白组不造模,其余2组予以闭合造模,造模成功后治伤巴布剂组在骨折标记部位予治伤巴布剂局部外敷;模型组则予等剂量赋形剂局部外敷(每天换药一次),干预7 d。造模后分别于1、3、7 d 3个时相点观测大鼠骨折肢体肿胀度、苏木精-伊红染色法(HE)观察骨折断端病理形态变化、酶联免疫吸附试验(ELISA)检测血清中TNF-α水平。结果表明:(1)与空白组对比,模型组及治伤巴布剂组在1、3、7 d 3个时相点大鼠右侧股骨明显肿胀(P<0.01),治伤巴布剂组在1、3、7 d 3个时相点肢体肿胀度较模型组明显减轻(P<0.01)。(2)HE染色结果显示模型组中可见少量软骨细胞和肉芽组织,未见骨小梁形成;治伤巴布剂可见大量软骨细胞和肉芽组织,并可见少量骨小梁形成。(3)ELISA结果显示与空白组相比,模型组及治伤巴布剂组TNF-α水平明显升高(P<0.01);与模型组相比,治伤巴布剂组TNF-α水平明显降低(P<0.01)。治伤巴布剂可以减轻大鼠股骨中段的肿胀度,对骨折的早期愈合具有一定促进作用,且降低TNF-α浓度水平抑制炎症反应。展开更多
文摘As a main pro-inflammatory factor, the up-regulation of TNF-α in RA patients plays a pivotal role in RA pathogenesis. The process of TNF production starts with the binding of a ligand( which is commonly a microbial product) to a cell surface Toll receptor, which stimulates a signal transduction pathway that activates NF - κB transcription factors. Activated NF - κB enters nuclei and induces the transcription of genes associated with inflammation, including those coding for TNF. The production of TNF and other inflammatory cytokines serves to recruit other inflammatory cells, which in turn release cytokines and subsequently amplify the immune response. TNF exerts its effect via binding of TNFRland TNFR2 receptors. Many experimental and clinical study have proved the effectiveness of TNF - αa ctivity blockade. Recent therapeutic interventions, including TNF - α and IL - 1 inhibitors, strongly support the importance of cytokines in RA. The mechanism of anti - TNF - α action in vivo is complex and probably includes suppression of other pro - inflammatory cytokines, decreased synovial cellular infiltration, interference with osteoclast activation, and decreased angiogenisis. Studies using anti -TNF agents clearly show that they can slow or prevent the progression of bone and cartilage damage in RA. This activity probably involves suppression of osteoclasts in joint lesions. Etanereept, Infliximab and adalimumab are the three main biologic agents that were fo-cused on clinically at present.
文摘为了研究治伤巴布剂对大鼠早期骨折愈合及对肿瘤坏死因子-α(tumornecrosisfactor-α,TNF-α)表达的影响,将45只SPF级雄性大鼠随机分为空白组、模型组、治伤巴布剂组3个组,每组15只。空白组不造模,其余2组予以闭合造模,造模成功后治伤巴布剂组在骨折标记部位予治伤巴布剂局部外敷;模型组则予等剂量赋形剂局部外敷(每天换药一次),干预7 d。造模后分别于1、3、7 d 3个时相点观测大鼠骨折肢体肿胀度、苏木精-伊红染色法(HE)观察骨折断端病理形态变化、酶联免疫吸附试验(ELISA)检测血清中TNF-α水平。结果表明:(1)与空白组对比,模型组及治伤巴布剂组在1、3、7 d 3个时相点大鼠右侧股骨明显肿胀(P<0.01),治伤巴布剂组在1、3、7 d 3个时相点肢体肿胀度较模型组明显减轻(P<0.01)。(2)HE染色结果显示模型组中可见少量软骨细胞和肉芽组织,未见骨小梁形成;治伤巴布剂可见大量软骨细胞和肉芽组织,并可见少量骨小梁形成。(3)ELISA结果显示与空白组相比,模型组及治伤巴布剂组TNF-α水平明显升高(P<0.01);与模型组相比,治伤巴布剂组TNF-α水平明显降低(P<0.01)。治伤巴布剂可以减轻大鼠股骨中段的肿胀度,对骨折的早期愈合具有一定促进作用,且降低TNF-α浓度水平抑制炎症反应。
