Jiang Xiao-Ming, Hu Jing-Hai, Wang Lu-Lu, Ma Chi, Wang Xu, Liu Xiao-Liang
Department of Emergency Medicine, The First Hospital of Jilin University Changchun, Jilin 130021, P.R. China.
Department of Urology, The First Hospital of Jilin University Changchun, Jilin 130021, P.R. China.
Transl Neurosci. 2016 Nov 24;7(1):158-163. doi: 10.1515/tnsci-2016-0023. eCollection 2016.
Ulinastatin [urinary trypsin inhibitor (UTI)] plays an important role in the protection of organs against ischemic injury during severe inflammation. The purposes of this study were to examine the effects of UTI on the levels of pro-inflammatory cytokines (PICs) and protein expression of PIC receptors in the neocortex and hippocampus CA1 region of rats after transient global ischemia induced via cardiac arrest (CA). Specifcally, interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were analyzed. CA was induced by asphyxia followed by cardiopulmonary resuscitation in rats. ELISA and western blot analysis were employed to determine PICs and their receptors in the neocortex and hippocampus. Our results show that IL-1β, IL-6 and TNF-α were significantly elevated in the neocortex and hippocampal CA1 field after CA. This was accompanied with an increase in PIC receptors, namely IL-1R, IL-6R and TNFR1. Systemic injection of UTI attenuated the amplification of PIC signal pathways in these brain regions. UTI also improved the modified Neurological Severity Score and brain tissue edema in CA rats. Notably, UTI resulted in an increase in survival of CA rats as compared to CA rats without treatment. In conclusion, UTI plays a beneficial role in modulating transient global ischemia induced by CA by altering PIC signal mechanisms, but further studies are needed to draw more firm conclusions.
乌司他丁[尿胰蛋白酶抑制剂(UTI)]在严重炎症期间保护器官免受缺血性损伤中起着重要作用。本研究的目的是检测乌司他丁对心脏骤停(CA)诱导的短暂全脑缺血后大鼠新皮质和海马CA1区促炎细胞因子(PICs)水平及PIC受体蛋白表达的影响。具体分析了白细胞介素-1β(IL-1β)、白细胞介素-6(IL-6)和肿瘤坏死因子-α(TNF-α)。通过窒息诱导大鼠心脏骤停,随后进行心肺复苏。采用酶联免疫吸附测定(ELISA)和蛋白质印迹分析来测定新皮质和海马中的PICs及其受体。我们的结果显示,心脏骤停后新皮质和海马CA1区的IL-1β、IL-6和TNF-α显著升高。这伴随着PIC受体即IL-1R、IL-6R和TNFR1的增加。全身注射乌司他丁减弱了这些脑区PIC信号通路的放大。乌司他丁还改善了心脏骤停大鼠的改良神经功能缺损评分和脑组织水肿。值得注意的是,与未治疗的心脏骤停大鼠相比,乌司他丁提高了心脏骤停大鼠的存活率。总之,乌司他丁通过改变PIC信号机制在调节心脏骤停诱导的短暂全脑缺血中发挥有益作用,但需要进一步研究以得出更确凿的结论。