Zheng Y, Song T, Zhang Ll, Wei N
Department of Geriatrics, First Affiliated Hospital of Harbin Medical University, Harbin City, P.R. China.
J Biol Regul Homeost Agents. 2018 Jan-Feb;32(1):29-35.
The aim of the present study was to analyze the relationship between cerebral ischemia and immune effects. A total of 70 Kunming mice were randomly divided into two groups: a model group (60 mice) and a sham group (10 mice). The model group was divided into six subgroups (10 mice per group) which were categorized according to the following time periods of treatment: 6 h, 12 h, 24 h, 48 h, 72 h and 5 days. The temporary middle cerebral artery occlusion (tMCAO) mouse model was established using intracavitary suture. The degree of brain injury was evaluated by detecting the neurological deficit score (NDS). Following cerebral ischemia reperfusion, the edema of the brain tissue was aggravated, and the infarction area was increased. At 48 h, the volume of the cerebral infarction reached a peak (44.4±3.2%) and then it decreased. The NDS score gradually decreased, and the nerve function was gradually restored. At 6 h, the NDS score was 4.6±0.55, whereas at the 5 d time point, it was significantly decreased (P less than 0.05) to 2.2±0.45. Flow cytometry analysis indicated that the percentage of Th17 cells increased gradually following ischemia. At 24 h, the percentage of Th17 cells reached its maximum value (0.70±0.10%) compared with the sham and the 5 d groups (P less than 0.05). At 24 h, the percentage of Th17 cells reached the lowest value (0.9±0.29%), whereas at the 5 d time point it increased significantly (3.2±0.49%) compared with the normal level (P less than 0.05). The secretion of Th17 and Treg-associated cytokines was consistent with the number of Th17 and Treg cells following ischemia. However, the levels of IL-17A in the brain tissues and the serum indicated a tendency to increase following the prolongation of ischemia. This marker reached the maximum levels on day 5. The IL-17 brain level was 77.9±5.11pg/ml, whereas the serum level was 29.44±3.06pg/ml. The changes in the secretion of the Th17 and Treg-related inflammatory cytokines were consistent with the changes in the cell ratio of Th17 and Treg cells. A significant correlation was noted between the two groups and the degree of ischemic brain injury. The results suggested that the functional status of Th17/Treg cells was imbalanced following cerebral ischemia.
本研究的目的是分析脑缺血与免疫效应之间的关系。总共70只昆明小鼠被随机分为两组：模型组（60只小鼠）和假手术组（10只小鼠）。模型组又分为六个亚组（每组10只小鼠），根据以下治疗时间段进行分类：6小时、12小时、24小时、48小时、72小时和5天。采用腔内缝合线建立暂时性大脑中动脉闭塞（tMCAO）小鼠模型。通过检测神经功能缺损评分（NDS）评估脑损伤程度。脑缺血再灌注后，脑组织水肿加重，梗死面积增大。在48小时时，脑梗死体积达到峰值（44.4±3.2%），然后下降。NDS评分逐渐降低，神经功能逐渐恢复。在6小时时，NDS评分为4.6±0.55，而在5天时间点，显著降低（P小于0.05）至2.2±0.45。流式细胞术分析表明，缺血后Th17细胞百分比逐渐增加。在24小时时，与假手术组和5天组相比，Th17细胞百分比达到最大值（0.70±0.10%）（P小于0.05）。在24小时时，Th17细胞百分比达到最低值（0.9±0.29%），而在5天时间点，与正常水平相比显著增加（3.2±0.49%）（P小于0.05）。缺血后Th17和Treg相关细胞因子的分泌与Th17和Treg细胞数量一致。然而，脑组织和血清中IL-17A水平显示随着缺血时间延长有升高趋势。该标志物在第5天达到最高水平。脑内IL-17水平为77.9±5.11pg/ml，而血清水平为29.44±3.06pg/ml。Th17和Treg相关炎性细胞因子分泌的变化与Th17和Treg细胞的细胞比例变化一致。两组之间与缺血性脑损伤程度存在显著相关性。结果表明，脑缺血后Th17/Treg细胞的功能状态失衡。
