Su Y, Fan W, Ma Z, Wen X, Wang W, Wu Q, Huang H
The Graduate School, Tianjin Medical University, Tianjin 300070, PR China.
Tianjin Neurosurgical Institute, Tianjin Huanhu Hospital, Tianjin 300060, PR China.
Neuroscience. 2014 Apr 25;266:56-65. doi: 10.1016/j.neuroscience.2014.02.006. Epub 2014 Feb 14.
We investigated the effect of taurine on inflammatory cytokine expression, on astrocyte activity and cerebral edema and functional outcomes, following traumatic brain injury (TBI) in rats. 72 rats were randomly divided into sham, TBI and Taurine groups. Rats subjected to moderate lateral fluid percussion injury were injected intravenously with taurine (200mg/kg) or saline immediately after injury or daily for 7days. Functional outcome was evaluated using Modified Neurological Severity Score (mNSS). Glial fibrillary acidic protein (GFAP) of the brain was measured using immunofluorescence. Concentration of 23 cytokines and chemokines in the injured cortex at 1 and 7days after TBI was assessed by Luminex xMAP technology. The results showed that taurine significantly improved functional recovery except 1day, reduced accumulation of GFAP and water content in the penumbral region at 7days after TBI. Compared with the TBI group, taurine significantly suppressed growth-related oncogene (GRO/KC) and interleukin (IL)-1β levels while elevating the levels of regulated on activation, normal T cell expressed and secreted (RANTES) at 1day. And taurine markedly decreased the level of 17 cytokine: eotaxin, Granulocyte colony-stimulating factor (G-CSF), Granulocyte-macrophage colony-stimulating factor (GM-CSF), interferon-gamma (IFN-γ), IL-1α, IL-1β, IL-4, IL-5, IL-6, IL-10, IL-12p70, IL-13, IL-17, leptin, monocyte chemotactic protein-1 (MCP-1), tumor necrosis factor-alpha (TNF-α), vascular endothelial growth factor (VEGF), and only increased the level of MIP-1α in a week. The results suggest that taurine effectively mitigates the severity of brain damage in TBI by attenuating the increase of astrocyte activity and edema as well as pro-inflammatory cytokines.
我们研究了牛磺酸对大鼠创伤性脑损伤(TBI)后炎性细胞因子表达、星形胶质细胞活性、脑水肿及功能结局的影响。72只大鼠随机分为假手术组、TBI组和牛磺酸组。中度侧方流体冲击伤大鼠在伤后立即静脉注射牛磺酸(200mg/kg)或生理盐水,或每日注射,共7天。使用改良神经功能缺损评分(mNSS)评估功能结局。采用免疫荧光法检测脑内胶质纤维酸性蛋白(GFAP)。通过Luminex xMAP技术评估TBI后1天和7天损伤皮质中23种细胞因子和趋化因子的浓度。结果显示,除第1天外,牛磺酸显著改善了功能恢复,降低了TBI后7天半暗带区域GFAP的积累和含水量。与TBI组相比,牛磺酸在第1天显著抑制生长相关癌基因(GRO/KC)和白细胞介素(IL)-1β水平,同时提高调节激活正常T细胞表达和分泌因子(RANTES)水平。牛磺酸显著降低了17种细胞因子水平:嗜酸性粒细胞趋化因子、粒细胞集落刺激因子(G-CSF)、粒细胞-巨噬细胞集落刺激因子(GM-CSF)、干扰素-γ(IFN-γ)、IL-1α、IL-1β、IL-4、IL-5、IL-6、IL-10、IL-12p70、IL-13、IL-17、瘦素、单核细胞趋化蛋白-1(MCP-1)、肿瘤坏死因子-α(TNF-α)、血管内皮生长因子(VEGF),且在一周内仅提高了MIP-1α水平。结果表明,牛磺酸通过减轻星形胶质细胞活性增加、水肿以及促炎细胞因子的产生,有效减轻了TBI后脑损伤的严重程度。