丙泊酚联合缺氧诱导因子和炎性小体抑制复杂区域疼痛综合征的镇痛作用研究
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The analgesic effect of propofol associated with the inhibition of hypoxia inducible factor and inflammasome in complex regional pain syndrome
背景与目的
复杂区域疼痛综合征（CRPS）与组织缺氧引起的微循环障碍和受累肢体外周血细胞因子过度生成有关，慢性缺血后疼痛（CPIP）被认为是该难治性疾病的动物模型。以往的研究表明，CPIP的发病机制包括缺氧诱导因1α（HIF-1α）及过度的局部炎症和自由基反应。由于HIF-1α的抑制作用可以减轻CPIP，因此异丙酚作为自由基清除剂，在缓解CPIP方面很可能是有用的。
方 法
我们用小鼠下肢建立CPIP模型。我们在再灌注期（早期）和第二天（晚期）分别给予异丙酚（10mg/kg）作为治疗。分析评估HIF-1α、自由基和炎症小体的表达。
结 果
丙泊酚在CPIP早期（再灌注后2小时）的行为学和热学评价中均产生明显的镇痛作用。仅在晚期(再灌注后48小时)有轻微的镇痛作用。早期，异丙酚可抑制缺氧诱导因子-1α（HIF-1α）、炎症标志物（NALP1）和半胱氨酸蛋白酶-1（caspase-1）的表达。并且在丙泊酚组中自由基水平也是降低的。但这些分子变化在CPIP的晚期并没有发现。
结 论
丙泊酚在CPIP早期对小鼠产生镇痛作用，其作用与抑制自由基、低氧诱导因子和炎性小体有关。
原始文献摘要
Hung-Tsung Hsiao, Yuan-Yuarn Liu, Jeffrey Chi-Fei Wang；The analgesic effect of propofol associated with the inhibition of hypoxia inducible factor and inflammasome in complex regional pain syndrome.[J] Journal of Biomedical Science, 2019,10,26:74
Background: Complex regional pain syndrome (CRPS) is related to microcirculation impairment caused by tissue hypoxia and peripheral cytokine overproduction in the affected human limb and chronic post-ischemic pain (CPIP) is considered as an animal model for this intractable disease. Previous studies suggest that the pathogenesis of CPIP involves the hypoxia inducible factor-1α (HIF-1α) and an exaggerated regional inflammatory and free radical response.The inhibition of HIF-1α is known to relieve CPIP. So, propofol, as a free radical scavenger, is very likely to be beneficial in terms of relieving CPIP.
Methods: We set up a CPIP model using the hindpaw of mice. We administered propofol (10 mg/kg) just after the reperfusion period (early stage) and also on the second day (late stage), as treatment. The analysis evaluated the expression of HIF-1α, free radicals, and inflammasome.
Results: Propofol administration produced obvious analgesia in both mechanical and thermal evaluation in the early stage of CPIP (2 h after reperfusion). Only a mild analgesic effect was found in the late stage (48 h later after reperfusion). In the early stage, the expression of HIF-1α and the inflammasome marker (NALP1) along with caspase-1 were suppressed by propofol. The free radical level also decreased in the propofol group. But those molecular changes were not founded in the late stage of CPIP.
Conclusion: Our data demonstrated that propofol produces mice analgesia in the early stage of CPIP and this effect is associated with inhibition of free radical, hypoxia inducible factor and inflammasome.
麻醉学文献进展分享
贵州医科大学高鸿教授课题组
翻译：唐剑 编辑：何幼芹 审校：王贵龙