Inhibitory effect on cerebral inflammatory response following traumatic brain injury in rats: a potential neuroprotective mechanism of N-acetylcysteine.
Inhibitory effect on cerebral inflammatory response following traumatic brain injury in rats: a potential neuroprotective mechanism of N-acetylcysteine.
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大鼠创伤性脑损伤后对脑炎症反应的抑制作用：N-乙酰半胱氨酸的潜在神经保护机制。
DOI：
10.1155/2008/716458
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发表时间：
2008
影响因子：
4.6
通讯作者：
Hang, Chunhua
中科院分区：
文献类型：
--
作者：
Chen, Gang;Shi, Jixin;Hu, Zhigang;Hang, Chunhua
尽管N-乙酰半胱氨酸（NAC）已被证明对创伤性脑损伤（TBI）具有神经保护作用，但这种有益作用的机制仍知之甚少。脑组织炎症在颅脑损伤后继发性脑损伤的发病机制中起重要作用。然而，尚未研究NAC是否调节TBI诱导的脑炎症反应。在这项工作中，我们研究了NAC给药对TBI后皮质核因子κ B（NF-κB）和炎症蛋白如白细胞介素-1 β（IL-1β）、肿瘤坏死因子-α（TNF-α）、白细胞介素-6（IL-6）和细胞间粘附分子-1（ICAM-1）表达的影响。结果，我们发现NF-κB、促炎细胞因子和ICAM-1在所有损伤动物中均升高。在TBI后给予NAC的动物中，与溶剂处理的动物相比，NF-κB、IL-1β、TNF-α和ICAM-1降低。NAC治疗后IL-6水平无明显变化。NAC给药可降低脑水肿、BBB通透性和损伤脑中的凋亡指数。结果表明，后TBI NAC管理可能会减弱在受伤的大鼠脑的炎症反应，这可能是一个机制，NAC改善继发性脑损伤后TBI。
Although N-acetylcysteine (NAC) has been shown to be neuroprotective for traumatic brain injury (TBI), the mechanisms for this beneficial effect are still poorly understood. Cerebral inflammation plays an important role in the pathogenesis of secondary brain injury after TBI. However, it has not been investigated whether NAC modulates TBI-induced cerebral inflammatory response. In this work, we investigated the effect of NAC administration on cortical expressions of nuclear factor kappa B (NF-κB) and inflammatory proteins such as interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and intercellular adhesion molecule-1 (ICAM-1) after TBI. As a result, we found that NF-κB, proinflammatory cytokines, and ICAM-1 were increased in all injured animals. In animals given NAC post-TBI, NF-κB, IL-1β, TNF-α, and ICAM-1 were decreased in comparison to vehicle-treated animals. Measures of IL-6 showed no change after NAC treatment. NAC administration reduced brain edema, BBB permeability, and apoptotic index in the injured brain. The results suggest that post-TBI NAC administration may attenuate inflammatory response in the injured rat brain, and this may be one mechanism by which NAC ameliorates secondary brain damage following TBI.
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影响因子：
4.2
作者：
Khan, M;Sekhon, B;Singh, AK
通讯作者：
Singh, AK
影响因子：
3.3
作者：
Knoblach, SM;Fan, L;Faden, AI
通讯作者：
Faden, AI
DOI：
10.1016/s0169-328x(98)00045-x
发表时间：
1998-05-01
期刊：
MOLECULAR BRAIN RESEARCH
影响因子：
--
作者：
Carroll, JE;Howard, EF;Cheng, C
通讯作者：
Cheng, C
影响因子：
4.6
作者：
Hoffer, E;Baum, Y;Nahir, AM
通讯作者：
Nahir, AM
影响因子：
5.5
作者：
Carlos, TM;Clark, RSB;Kochanekt, PM
通讯作者：
Kochanekt, PM