Hidmark Asa S, Nawroth Peter P, Fleming Thomas
Department of Medicine I and Clinical Chemistry, University Hospital of Heidelberg, INF 410, Heidelberg, Germany.
Department of Medicine I and Clinical Chemistry, University Hospital of Heidelberg, INF 410, Heidelberg, Germany; Institute for Diabetes and Cancer IDC Helmholtz Center Munich, Germany & Joint Heidelberg-IDC Translational Diabetes Program, Neuherberg, Germany; German Center for Diabetes Research (DZD), Ingolstädter Landstraße 1, 85764 Neuherberg, Germany.
J Neuroimmunol. 2017 May 15;306:76-82. doi: 10.1016/j.jneuroim.2017.03.008. Epub 2017 Mar 11.
Streptozotocin (STZ) treatment, a common model for inducing diabetes in rodent models, induces thermal hyperalgesia and neuronal toxicity independently of hyperglycemia by oxidizing and activating TRPA1 and TRPV1. Following treatment with STZ, CD45 immune cells were found to be depleted in sciatic nerve (SN) and DRG in mice, prior to hyperglycemia. Macrophages were also lost in DRG and NFκB-p65-activation was increased in SN macrophages. Immune cells were significantly reduced in both SN and DRG up to three weeks, post-treatment. Loss of PNS-resident macrophages in response to STZ-mediated toxicity may affect the regenerative capacity of the nerve in response to further injury caused by diabetes.
链脲佐菌素（STZ）治疗是在啮齿动物模型中诱导糖尿病的常见模型，它通过氧化和激活TRPA1和TRPV1，独立于高血糖诱导热痛觉过敏和神经元毒性。在用STZ治疗后，在小鼠坐骨神经（SN）和背根神经节（DRG）中，在高血糖出现之前就发现CD45免疫细胞减少。DRG中的巨噬细胞也减少，并且SN巨噬细胞中的NFκB-p65激活增加。治疗后长达三周，SN和DRG中的免疫细胞均显著减少。响应STZ介导的毒性，外周神经系统驻留巨噬细胞的丧失可能会影响神经对糖尿病引起的进一步损伤的再生能力。
