Fan Yue-Shan, Wang Bo, Wang Dong, Xu Xin, Gao Chuang, Li Ying, Zhang Shu, Yang Gui-Li, Liu Xiao, Jiang Rong-Cai, Zhang Jian-Ning
Department of Neurosurgery, General Hospital of Tianjin Medical University; Tianjin Neurological Institute, Key Laboratory of Post-Neuroinjury Neuro-repair and Regeneration in Central Nervous System, Ministry of Education and Tianjin City; Graduate School, Tianjin Medical University, Tianjin, China.
Department of Neurosurgery, Xuanwu Hospital, Capital Medical University, Beijing, China.
Neural Regen Res. 2021 Mar;16(3):523-530. doi: 10.4103/1673-5374.293152.
Atorvastatin has been shown to be a safe and effective non-surgical treatment option for patients with chronic subdural hematoma. However, treatment with atorvastatin is not effective in some patients, who must undergo further surgical treatment. Dexamethasone has anti-inflammatory and immunomodulatory effects, and low dosages are safe and effective for the treatment of many diseases, such as ankylosing spondylitis and community-acquired pneumonia. However, the effects of atorvastatin and low-dose dexamethasone for the treatment of chronic subdural hematoma remain poorly understood. Hematoma samples of patients with chronic subdural hematoma admitted to the General Hospital of Tianjin Medical University of China were collected and diluted in endothelial cell medium at 1:1 as the hematoma group. Atorvastatin, dexamethasone, or their combination was added to the culture medium. The main results were as follows: hopping probe ion conductance microscopy and permeability detection revealed that the best dosages to improve endothelial cell permeability were 0.1 μM atorvastatin and 0.1 μM dexamethasone. Atorvastatin, dexamethasone, or their combination could markedly improve the recovery of injured endothelial cells. Mice subcutaneously injected with diluted hematoma solution and then treated with atorvastatin, dexamethasone, or their combination exhibited varying levels of rescue of endothelial cell function. Hopping probe ion conductance microscopy, western blot assay, and polymerase chain reaction to evaluate the status of human cerebral endothelial cell status and expression level of tight junction protein indicated that atorvastatin, dexamethasone, or their combination could reduce subcutaneous vascular leakage caused by hematoma fluid. Moreover, the curative effect of the combined treatment was significantly better than that of either single treatment. Expression of Krüppel-like factor 2 protein in human cerebral endothelial cells was significantly increased, as was expression of the tight junction protein and vascular permeability marker vascular endothelial cadherin in each treatment group compared with the hematoma stimulation group. Hematoma fluid in patients with chronic subdural hematoma may damage vascular endothelial cells. However, atorvastatin combined with low-dose dexamethasone could rescue endothelial cell dysfunction by increasing the expression of tight junction proteins after hematoma injury. The effect of combining atorvastatin with low-dose dexamethasone was better than that of atorvastatin alone. Increased expression of Krüppel-like factor 2 may play an important role in the treatment of chronic subdural hematoma. The animal protocols were approved by the Animal Care and Use Committee of Tianjin Medical University of China on July 31, 2016 (approval No. IRB2016-YX-036). The study regarding human hematoma samples was approved by the Ethics Committee of Tianjin Medical University of China on July 31, 2018 (approval No. IRB2018-088-01).
阿托伐他汀已被证明是慢性硬膜下血肿患者安全有效的非手术治疗选择。然而,阿托伐他汀治疗对一些患者无效,这些患者必须接受进一步的手术治疗。地塞米松具有抗炎和免疫调节作用,低剂量对许多疾病如强直性脊柱炎和社区获得性肺炎的治疗是安全有效的。然而,阿托伐他汀和低剂量地塞米松治疗慢性硬膜下血肿的效果仍知之甚少。收集中国天津医科大学总医院收治的慢性硬膜下血肿患者的血肿样本,并以1:1的比例在内皮细胞培养基中稀释作为血肿组。将阿托伐他汀、地塞米松或其组合添加到培养基中。主要结果如下:跳跃探针离子电导显微镜和通透性检测显示,改善内皮细胞通透性的最佳剂量为0.1μM阿托伐他汀和0.1μM地塞米松。阿托伐他汀、地塞米松或其组合可显著改善受损内皮细胞的恢复。皮下注射稀释血肿溶液后再用阿托伐他汀、地塞米松或其组合治疗的小鼠,内皮细胞功能的挽救程度各不相同。通过跳跃探针离子电导显微镜、蛋白质印迹分析和聚合酶链反应评估人脑内皮细胞状态和紧密连接蛋白表达水平,结果表明阿托伐他汀、地塞米松或其组合可减少血肿液引起的皮下血管渗漏。此外,联合治疗的疗效明显优于单一治疗。与血肿刺激组相比,各治疗组人脑内皮细胞中Krüppel样因子2蛋白的表达显著增加,紧密连接蛋白和血管通透性标志物血管内皮钙黏蛋白的表达也显著增加。慢性硬膜下血肿患者的血肿液可能会损伤血管内皮细胞。然而,阿托伐他汀联合低剂量地塞米松可通过增加血肿损伤后紧密连接蛋白的表达来挽救内皮细胞功能障碍。阿托伐他汀联合低剂量地塞米松的效果优于单独使用阿托伐他汀。Krüppel样因子2表达的增加可能在慢性硬膜下血肿的治疗中起重要作用。动物实验方案于2016年7月31日获得中国天津医科大学动物护理和使用委员会批准(批准号IRB2016-YX-036)。关于人类血肿样本的研究于2018年7月31日获得中国天津医科大学伦理委员会批准(批准号IRB2018-088-01)。