| 秦传子,姜维良,陈 波,王海涛,孙占峰,马 军.NLRP3炎性小体及其下游产物在TAO和ASO患者动脉中的表达及意义[J].现代生物医学进展英文版,2018,(9):1687-1693. |
| NLRP3炎性小体及其下游产物在TAO和ASO患者动脉中的表达及意义 |
| The Expressions and Significances of NLRP3 Inflammasome and its Downstream Products in the Treatment of Arteries of Patients with TAO and ASO |
| Received:November 28, 2017 Revised:January 03, 2018 |
| DOI：10.13241/j.cnki.pmb.2018.09.018 |
| 中文关键词: NLRP3炎性小体 血栓闭塞性脉管炎 下肢动脉硬化性闭塞症 |
| 英文关键词: NLRP3 inflammasome Thromboangiitis obliterans Arteriosclerosis obliterans |
| 基金项目:黑龙江省青年科学基金项目（QC2013C115） |
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| 中文摘要: |
| 摘要 目的：探讨NLRP3炎性小体及其下游产物在血栓闭塞性脉管炎(TAO)和动脉粥样硬化闭塞症(ASO)患者动脉中的表达及意义。方法：选择8例TAO患者截肢后的下肢动脉，13例ASO患者截肢后的下肢动脉，5例因窒息死亡的新生儿主动脉，将三组动脉分别进行HE染色及免疫组化分析，半定量的测量3组动脉中NLRP3、Caspase-1、IL-1β和IL-18的累积光密度值(IOD)并进行组间比较。结果：3组动脉组织的HE染色结果均符合其特征。TAO组和ASO组动脉组织中NLRP3、Caspase-1、IL-1β和IL-18的表达与对照组相比均显著升高，差异具有统计学意义(P＜0.05)。结论：NLRP3、Caspase-1、IL-1β和IL-18在TAO和ASO患者动脉组织中的表达明显升高，NLRP3炎性小体及其下游产物可能参与了TAO和ASO的发病过程。 |
| 英文摘要: |
| ABSTRACT Objective: To investigate the expression and significance of NLRP3 inflammasome and its downstream products in the arteries of patients with Thromboangiitis obliterans and Arteriosclerosis obliterans. Methods: Selected the arteries from 8 amputation pa- tients who with TAO , The arteries from 13 amputation patients who with ASO, The arteries from 5 neonates who death by suffocation.The 3 groups arteries were analyzed by hematoxylin-eosin staining and immunohistochemistry. Semi quantitative measurement the NL- RP3, Caspase-1, IL-1β and IL-18 protein in the 3 groups by the Integrated Option Density (IOD). Calculate its average As its relative ex- pression. Results: The HE staining results of the three groups of arteries accorded with their characteristics. The expressions of NLRP3, Caspase-1, IL-1β and IL-18 in the arterial tissues of group TAO and group ASO were significantly higher than those of the control group. The difference was statistically significant (P<0.05). Conclusion: The expression of NLRP3, Caspase-1, IL-1β and IL-18 in the arterial tissues of patients with TAO and ASO increased significantly. NLRP3 inflammasome and its downstream products may be in- volved in the pathogenesis of TAO and ASO. |
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