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Hypothermic intervention for 3 hours inhibits apoptosis in neonatal rats with hypoxic-ischemic brain damage

机译:低温治疗3小时可抑制缺氧缺血性脑损伤新生大鼠的细胞凋亡

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摘要

A neonatal rat model of hypoxic-ischemic brain damage was designed and implemented in this study. Rats were subjected to hypothermia at 31?C immediately following hypoxia-ischemia for either 3, 6 or 15 hours. TdT-mediated dUTP nick end labeling demonstrated that the number of apoptotic cells was reduced in the rat cerebral cortex, hippocampus and periventricular white matter following hypothermia. Immunohistochemistry revealed that Bcl-2 and p16 expression were decreased. Inhibition of apoptosis was greatest with the 3 hour hypothermic treatment, followed by hypothermia for 6 hours. In contrast, hypothermia for 15 hours led to a decrease in neuronal number in the cerebral cortex. The results demonstrate that hypothermic intervention at 31?C protects brain tissue against hypoxic-ischemic brain damage by inhibiting apoptosis, and that the optimal length of treatment is 3 hours.
机译:在本研究中设计并实施了新生鼠缺氧缺血性脑损伤模型。缺氧缺血后3、6或15小时,立即在31℃对大鼠进行低温治疗。 TdT介导的dUTP缺口末端标记表明,低温后大鼠大脑皮质,海马和脑室周围白质中凋亡细胞的数量减少。免疫组织化学显示Bcl-2和p16表达降低。低温治疗3小时后,对细胞凋亡的抑制作用最大,然后进行低温6小时。相比之下,体温过低15小时会导致大脑皮层神经元数量减少。结果表明,在31°C下进行低温干预可通过抑制细胞凋亡来保护脑组织免于缺氧缺血性脑损伤,并且最佳治疗时间为3小时。

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