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Elevation of Pro-inflammatory and Anti-inflammatory Cytokines in Rat Serum after Acute Methamphetamine Treatment and Traumatic Brain Injury
Journal of Molecular Neuroscience ( IF 3.1 ) Pub Date : 2021-09-20 , DOI: 10.1007/s12031-021-01886-8
Firas H. Kobeissy 1, 2, 3 , Zaynab Shakkour 1 , Kevin K. W. Wang 2, 3 , Samer El Hayek 4 , Wael Mohamed 5, 6 , Mark S. Gold 7
Affiliation  

The use of methamphetamine (METH) is a growing worldwide epidemic that bears grave societal implications. METH is known to exert its neurotoxic effects on the dopaminergic and serotonergic systems of the brain. In addition to this classical studied mechanism of damage, findings from our laboratory and others have shown that acute METH treatment and mechanical injury, i.e. traumatic brain injury (TBI), share common cell injury mechanism(s). Since neuro-inflammation is a signature event in TBI, we hypothesize that certain cytokine levels might also be altered in rat brain exposed to an acute METH insult. In this study, using a cytokine antibody array chip, we evaluated the serum levels of 19 cytokines in rats 24 h after exposure to a 40 mg/kg acute regimen of METH. Data were compared to rats subjected to experimental TBI using the controlled cortical impact (CCI) injury model and saline controls. Sandwich ELISA method was used to further validate some of the findings obtained from the antibody cytokine array. We confirmed that three major inflammatory-linked cytokines (IL-1β, IL-6, and IL-10) were elevated in the METH and TBI groups compared to the saline group. Such finding suggests the involvement of an inflammatory process in these brain insults, indicating that METH use is, in fact, a stressor to the immune system where systemic involvement of an altered cytokine profile may play a major role in mediating chemical brain injury after METH use.



中文翻译:

急性甲基苯丙胺治疗和创伤性脑损伤后大鼠血清促炎和抗炎细胞因子的升高

甲基苯丙胺 (METH) 的使用是一种日益严重的全球流行病,具有严重的社会影响。已知 METH 对大脑的多巴胺能和血清素能系统发挥其神经毒性作用。除了这种经典的损伤机制研究之外,我们实验室和其他实验室的研究结果表明,急性 METH 治疗和机械损伤,即外伤性脑损伤 (TBI),具有共同的细胞损伤机制。由于神经炎症是 TBI 的标志性事件,我们假设暴露于急性 METH 损伤的大鼠大脑中某些细胞因子水平也可能发生改变。在这项研究中,我们使用细胞因子抗体阵列芯片评估了大鼠暴露于 40 mg/kg METH 急性治疗方案 24 小时后的 19 种细胞因子的血清水平。使用受控皮质撞击 (CCI) 损伤模型和盐水对照,将数据与经受实验性 TBI 的大鼠进行比较。夹心ELISA方法用于进一步验证从抗体细胞因子阵列获得的一些发现。我们证实,与盐水组相比,METH 和 TBI 组中三种主要的炎症相关细胞因子(IL-1β、IL-6 和 IL-10)升高。这一发现表明这些脑损伤中涉及炎症过程,表明 METH 的使用实际上是免疫系统的压力源,其中改变的细胞因子谱的全身参与可能在介导 METH 使用后的化学脑损伤中起主要作用. 我们证实,与盐水组相比,METH 和 TBI 组中三种主要的炎症相关细胞因子(IL-1β、IL-6 和 IL-10)升高。这一发现表明这些脑损伤中涉及炎症过程,表明 METH 的使用实际上是免疫系统的压力源,其中改变的细胞因子谱的全身性参与可能在介导 METH 使用后的化学脑损伤中起主要作用. 我们证实,与盐水组相比,METH 和 TBI 组中三种主要的炎症相关细胞因子(IL-1β、IL-6 和 IL-10)升高。这一发现表明这些脑损伤中涉及炎症过程,表明 METH 的使用实际上是免疫系统的压力源,其中改变的细胞因子谱的全身性参与可能在介导 METH 使用后的化学脑损伤中起主要作用.

更新日期:2021-09-21
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