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首页> 外文期刊>Injury >Effect of hypothermia on apoptosis in traumatic brain injury and hemorrhagic shock model
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Effect of hypothermia on apoptosis in traumatic brain injury and hemorrhagic shock model

机译：体温过低对创伤性脑损伤和出血休克模型凋亡的影响

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Abstract Introduction The neuroprotective mechanisms of therapeutic hypothermia against trauma-related injury have not been fully understood yet. In this study, we aimed to investigate the effects of therapeutic hypothermia on biochemical and histopathological markers of apoptosis using Traumatic brain injury (TBI) and hemorrhagic shock (HS) model. Methods A total of 50 male albino-wistar rats were divided into five groups: Group isolated TBI, Group NT (HT+HS+normothermia), Group MH (HT+HS+mild hypothermia), Group MoH (HT+HS+moderate hypothermia) and Group C (control). Neurological deficit scores were assessed at baseline and at 24h. The rats were, then, sacrificed to collect serum and brain tissue samples. Levels of Caspase-3,6,8, proteoglycan-4 (PG-4), malondialdehyde (MDA), and nitric oxide (NO) were measured in serum and brain tissue samples. Histopathological examination was performed in brain tissue. Results There were significant differences in the serum levels of Caspase-3 between Group NT and Group C (p=0.018). The serum levels of Caspase-6 in Group NT (0.70±0.58) were lower than Group MH (1.39±0.28), although the difference was not statistically significant (p=0.068). There were significant differences in the brain tissue samples for Caspase-3 levels between Group NT and Group C (p=0.049). A significant difference in the Caspase-8 brain tissue levels was also observed between Group NT and Group C (p=0.022). Group NT had significantly higher scores of all the pathological variables (for edema p Conclusion Our study results suggest that hypothermia may exert its neuroprotective effects by reducing markers of apoptotic pathway, particularly Caspase-3 on TBI and HS.
机译：摘要尚未完全理解介绍治疗性低温对创伤相关损伤的神经保护机制。在这项研究中，我们旨在使用创伤性脑损伤（TBI）和出血休克（HS）模型来研究治疗性低温对凋亡生物化学和组织病理学标志物的影响。方法将50只雄性白化Wistar大鼠分为五组：分离的TBI组，NT（HT + HS + Narothermia），MH（HT + HS +轻度体温过低），组MOH（HT + HS +中等低温）和c组（控制）。在基线和24小时内评估神经系统缺陷分数。然后，处死大鼠以收集血清和脑组织样品。在血清和脑组织样品中测量了Caspase-3,6,8，丙二糖-4（PG-4），丙二醛（MDA）和一氧化氮（NO）的水平。组织病理学检查在脑组织中进行。结果NT和C组之间的Caspase-3血清水平存在显着差异（p = 0.018）。 NT（0.70±0.58）组血清水平水平低于MH（1.39±0.28），尽管差异没有统计学意义（P = 0.068）。在NT和C组之间的Caspase-3水平的脑组织样品存在显着差异（p = 0.049）。在NT和C组之间也观察到Caspase-8脑组织水平的显着差异（p = 0.022）。 NT组的所有病理性变量的得分显着提高（对于水肿P结论我们的研究结果表明，体温过低可能通过减少凋亡途径的标志物，特别是Caspase-3在TBI和HS上施加其神经保护作用。

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