首页|利多卡因分娩镇痛调节MAPK信号通路对新生鼠缺氧的改善作用

利多卡因分娩镇痛调节MAPK信号通路对新生鼠缺氧的改善作用

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目的 探讨利多卡因分娩镇痛调节丝裂原活化蛋白激酶(MAPK)信号通路对新生鼠缺氧的改善作用.方法 10只孕鼠随机分为正常分娩组、分娩窒息组、利多卡因组、茴香霉素组、利多卡因+茴香霉素组,每组2只.除正常分娩组外,其他组大鼠均于妊娠第21天诱发分娩窒息,待孕鼠宫缩开始即将生产时,对孕鼠给药处理,正常分娩组、分娩窒息组、利多卡因组、茴香霉素组、利多卡因+茴香霉素组孕鼠分别娩出12、13、12、14、12只新生鼠,各组均纳入12只新生鼠用于后续研究.Morris水迷宫实验检测新生鼠逃避潜伏期、探索空间所用时间、穿越平台数;苏木精-伊红(H-E)染色检测新生鼠海马CA1区病理;透射电子显微镜观察新生鼠突触形态;试剂盒检测海马CA1区中丙二醛(MDA)、超氧化物歧化酶(SOD)水平;TUNEL染色检测海马CA1区神经元凋亡;Western blot检测海马CA1区中Bim、p53、p-p38MAPK、p-ERK蛋白.结果 与分娩窒息组相比,利多卡因组新生鼠逃避潜伏期、探索空间所用时间缩短,穿越平台数增加,海马CA1区病理损伤减轻,突触数量、突触小泡数目增多,突触后致密物厚度变厚,海马CA1区脑组织中MDA水平、神经元凋亡率、Bim、p53、p-p38 MAPK、p-ERK蛋白降低,SOD水平升高,茴香霉素组对应指标变化趋势与利多卡因组相反(P<0.05);茴香霉素逆转了利多卡因对分娩窒息组新生鼠的保护作用.结论 利多卡因分娩镇痛通过抑制MAPK/ERK信号通路改善新生鼠缺氧.
The ameliorating effect of lidocaine induced labor analgesia on hypoxia in neonatal rats by regulating the MAPK signaling pathway
Objective To investigate the ameliorating effect of lidocaine induced labor analgesia on hypoxia in neo-natal rats by regulating mitogen-activated protein kinase(MAPK)signaling pathway.Methods Ten pregnant rats were ran-domly grouped into normal delivery group,delivery asphyxia group,lidocaine group,anisemycin group,lidocaine+anisemycin group,with 2 rats in each group.Except for the normal delivery group,the rats in the other groups were induced asphyxia on the 21st day of pregnancy,and the pregnant rats were administered when the contractions began and the pregnant rats were about to give birth.A total of 12,13,12,14,and 12 newborn rats were delivered in the normal delivery group,the delivery asphyxia group,the lidocaine group,the animomycin group,and the lidocaine+anitomycin group,respectively,so 12 newborn rats were included in each group for follow-up studies.Morris water maze test was used to detect the escape latency,the time spent exploring space,and the number of times crossing platforms.H-E staining was used to detect the brain histopathology in the CA1 region of the hippocampus of neonatal rats.Transmission electron microscopy was used to observe the synaptic mor-phology of neonatal rats.Kits was used to detect the levels of malondialdehyde(MDA)and superoxide dismutase(SOD)in the CA1 region of hippocampus.TUNEL staining was used to detect neuronal apoptosis in the CA1 region of the hippocampus.Western blot was used to detect Bim,p53,p-p38 MAPK and p-ERK proteins in the CA1 of hippocampus.Results Compared with the delivery asphyxia group,the escape latency and time spent exploring space of newborn rats were shortened,the number of times crossing platforms was increased,pathological damage in hippocampal CA1 region was reduced,the numbers of syn-apses and synaptic vesicles increased,and the thickness of postsynaptic dense matter thickened,the levels of MDA,neuronal apoptosis rate,Bim,p53,p-p38 MAPK,and p-ERK proteins in the brain tissue of the hippocampal CA1 region decreased,the level of SOD increased in the lidocaine group,the trend of corresponding indexes in the animomycin group was opposite that in the lidocaine group(P<0.05).Anisinomycin reversed the protective effect of lidocaine on neonatal rats in the delivery as-phyxia group.Conclusion Lidocaine-induced labor analgesia improves neonatal hypoxia by inhibiting the MAPK/ERK sig-naling pathway.

lidocainelabor analgesianeonatal hypoxic-ischemic brain damageoxidative stressapoptosis

刘权、吴君如、桑子琼

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湖北民族大学附属民大医院麻醉手术中心,湖北恩施 445000

湖北民族大学附属民大医院产科,湖北恩施 445000

利多卡因 分娩镇痛 新生儿缺氧缺血性脑损伤 氧化应激 凋亡

2024

中国优生与遗传杂志
中国优生科学协会

中国优生与遗传杂志

CSTPCD
影响因子:0.527
ISSN:1006-9534
年,卷(期):2024.32(11)