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程亮亮,田 毅,谭义文,李美霞.基于 MAPK 信号通路七氟醚分娩镇痛对新生鼠缺氧的改善作用研究[J].中国比较医学杂志,2021,31(5):53~58.
基于 MAPK 信号通路七氟醚分娩镇痛对新生鼠缺氧的改善作用研究
Effect of sevoflurane analgesia on the mitogen-activated protein kinase signaling pathway during hypoxia in neonatal rats
投稿时间:2020-07-08  
DOI:10. 3969 / j.issn.1671-7856. 2021. 05. 009
中文关键词:  七氟醚  分娩镇痛  新生鼠  缺氧  丝裂原活化蛋白激酶
英文关键词:sevoflurane  labor analgesia  neonatal rat hypoxia  mitogen-activated protein kinase
基金项目:
作者单位E-mail
程亮亮 中南大学湘雅医学院附属海口医院麻醉与疼痛医学科,海口 570208 x245iao@ 163.com 
田 毅 中南大学湘雅医学院附属海口医院麻醉与疼痛医学科,海口 570208 13876826960@ 126.com 
谭义文 中南大学湘雅医学院附属海口医院麻醉与疼痛医学科,海口 570208  
李美霞 中南大学湘雅医学院附属海口医院麻醉与疼痛医学科,海口 570208  
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中文摘要:
       目的 探讨基于丝裂原活化蛋白激酶(MAPK)信号通路七氟醚分娩镇痛对新生鼠缺氧的改善作用。 方法 模型组、七氟醚组孕鼠建立分娩窒息模型,模型组给予 50%体积分数的氧气,七氟醚组给予体积分数 50%的氧气和 2. 5%七氟醚;自然分娩组自然分娩。 评估新生子鼠学习记忆能力,检测血清超氧化物歧化酶 (SOD)、丙二醛(MDA)水平、脑组织海马 CA1 区尼氏小体数目及脑组织 MAPK、B 细胞淋巴瘤-2 基因(Bcl-2)、Bcl-2 相关 X 蛋白(Bax)、半胱氨酸蛋白酶-3(Caspase-3)mRNA 和蛋白表达量。 结果 与模型组比较,七氟醚组新生子鼠目标象限停留时间延长,穿越平台次数增多,血清 SOD 升高,MDA 降低,海马 CA1 区尼氏小体数目增多,脑组织 Bcl-2 mRNA 和蛋白表达量及 Bcl-2/ Bax 升高,MAPK、Bax、Caspase-3 mRNA 和蛋白表达量降低,差异均有统计学意义(P<0. 05)。 结论 七氟醚分娩镇痛可有效改善新生鼠缺氧缺血脑损伤状况,可能通过抑制 MAPK 信号通路,进而抑制海马神经元损伤,发挥脑保护作用。
英文摘要:
       Objective To examine the effect of sevoflurane analgesia during hypoxia in neonatal rats on the mitogen-activated protein kinase ( MAPK) signaling pathway. Methods In the model group and sevoflurane group, pregnant rats were administered birth asphyxia models. The model group was administered 50% oxygen by volume, while the sevoflurane group was administered 50% oxygen and 2. 5% sevoflurane. The natural delivery group gave birth spontaneously. The learning and memory abilities of newborn ofFspring were assessed. Serum superoxide dismutase (SOD), malondialdehyde (MDA) levels, and number of Nissl bodies in the CA1 area of the hippocampus in brain tissue were examined. Brain tissue MAPK, B-cell lymphoma-2 gene (Bcl-2), Bcl-2 related X protein (Bax), and cysteine protease-3 (caspase-3) mRNA and protein expression were also examined. Results Compared with the model group, newborn ofFspring in the sevoflurane group showed a longer residence time in the target quadrant, increased number of crossing platforms, increased serum SOD, decreased MDA, increased number of Nissl bodies in the hippocampal CA1 area, and increased expression of Bcl-2 mRNA and protein in brain tissue. Expression of MAPK, Bax, and caspase-3 mRNA and protein was decreased (P< 0.05). Conclusions Sevoflurane labor analgesia can effectively improve hypoxic-ischemic brain damage in neonatal rats. It may play a protective role in the brain by inhibiting the MAPK signaling pathway and in turn inhibiting hippocampal neuron damage.
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