Hypothermia modulates cytokine responses after neonatal rat hypoxic-ischemic injury and reduces brain damage.
Hypothermia modulates cytokine responses after neonatal rat hypoxic-ischemic injury and reduces brain damage.
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DOI：
10.1177/1759091414558418
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发表时间：
2014
期刊：
影响因子：
4.7
通讯作者：
Ashwal S
中科院分区：
文献类型：
--
作者：
Yuan X;Ghosh N;McFadden B;Tone B;Bellinger DL;Obenaus A;Ashwal S
虽然低温（HT）是新生儿缺氧缺血性损伤（HII）的标准治疗方法，但其神经保护作用的机制尚不清楚。我们在 10 日龄的 HII 幼鼠模型中检查了缺血核心/半暗带和细胞因子/趋化因子的演变。 HII后，幼崽接受HT（32℃；n = 18）或常温（NT，35℃；n = 15）治疗24小时。结果包括磁共振成像 (MRI)、神经行为测试和脑细胞因子/趋化因子分析（HII 后 0、24、48 和 72 小时）。 HT 幼崽中的病变体积（24 小时）减少（总计 74%，p< .05；半影 68%，p< .05；核心 85%，p = .19）。病变体积在 72 小时（HT 后 48 小时）反弹，NT 和 HT 幼仔之间没有显着差异。 HT 在所有时间点都会降低白细胞介素 1β (IL-1β) (p < .05)；单核细胞趋化蛋白-1 (MCP-1) 在 HT 幼崽中呈下降趋势 (p = .09)。 HT 不会改变干细胞信号分子基质细胞衍生因子 1 (SDF-1)。我们的数据表明，HT 可能通过减少 IL-1β 而不影响 SDF-1 来减少总病变体积和半影病变体积（24 小时和 48 小时）。当IL-1β水平仍然较低时，HII后48至72小时HII体积的增加趋势之间的分离表明，复温后，与IL-1β表达无关的机制可能导致这种损伤的延迟增加。应考虑进行更多研究来确定这些机制可能是什么，并探讨延长 HT 的持续时间或程度是否可以改善这种延迟性损伤的增加。
While hypothermia (HT) is the standard-of-care for neonates with hypoxic ischemic injury (HII), the mechanisms underlying its neuroprotective effect are poorly understood. We examined ischemic core/penumbra and cytokine/chemokine evolution in a 10-day-old rat pup model of HII. Pups were treated for 24 hr after HII with HT (32℃; n = 18) or normothermia (NT, 35℃; n = 15). Outcomes included magnetic resonance imaging (MRI), neurobehavioral testing, and brain cytokine/chemokine profiling (0, 24, 48, and 72 hr post-HII). Lesion volumes (24 hr) were reduced in HT pups (total 74%, p < .05; penumbra 68%, p < .05; core 85%, p = .19). Lesion volumes rebounded at 72 hr (48 hr post-HT) with no significant differences between NT and HT pups. HT reduced interleukin-1β (IL-1β) at all time points (p < .05); monocyte chemoattractant protein-1 (MCP-1) trended toward being decreased in HT pups (p = .09). The stem cell signaling molecule, stromal cell-derived factor-1 (SDF-1) was not altered by HT. Our data demonstrate that HT reduces total and penumbral lesion volumes (at 24 and 48 hr), potentially by decreasing IL-1β without affecting SDF-1. Disassociation between the increasing trend in HII volumes from 48 to 72 hr post-HII when IL-1β levels remained low suggests that after rewarming, mechanisms unrelated to IL-1β expression are likely to contribute to this delayed increase in injury. Additional studies should be considered to determine what these mechanisms might be and also to explore whether extending the duration or degree of HT might ameliorate this delayed increase in injury.
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影响因子：
48
作者：
Rutherford, Mary;Ramenghi, Luca A.;Edwards, A. David;Brocklehurst, Peter;Halliday, Henry;Levene, Malcolm;Strohm, Brenda;Thoresen, Marianne;Whitelaw, Andrew;Azzopardi, Denis
通讯作者：
Azzopardi, Denis
影响因子：
11.2
作者：
Obenaus, Andre;Dilmac, Nejmi;Tone, Beatriz;Tian, Hou Rou;Hartman, Richard;Digicaylioglu, Murat;Snyder, Evan Y.;Ashwal, Stephen
通讯作者：
Ashwal, Stephen
DOI：
10.1073/pnas.0404474101
发表时间：
2004-08-10
影响因子：
11.1
作者：
Kelly, S;Bliss, TM;Steinberg, GK
通讯作者：
Steinberg, GK
影响因子：
6.2
作者：
Pinteaux, E;Rothwell, NJ;Boutin, H
通讯作者：
Boutin, H
影响因子：
6.3
作者：
Recker, Rebecca;Adami, Arash;Ashwal, Stephen
通讯作者：
Ashwal, Stephen