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PI3K/Akt通路对丙泊酚麻醉诱发大鼠脑损伤的影响 被引量:1

Effects of PI3K/Akt pathway on brain injury induced by propofol anesthesia in rats
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摘要 目的观察磷脂酰肌醇-3-激酶(PI3K)/蛋白激酶B(Akt)通路对丙泊酚麻醉诱发大鼠脑损伤的影响。方法2020年3月—2021年4月在恩施土家族苗族自治州中心医院进行丙泊酚麻醉诱发大鼠脑损伤实验,取SD大鼠30只,随机数字表法分为对照组、2%丙泊酚组、4%丙泊酚组,各10只。2%丙泊酚组、4%丙泊酚组大鼠分别予相应浓度丙泊酚造模,对照组仅予1%氯化钠肌肉注射。连续干预4 d后比较各组大鼠学习记忆能力、血清炎性因子[肿瘤坏死因子-α(TNF-α)、白介素1β(IL-1β)]、脑组织PI3K/Akt通路蛋白表达情况。结果对照组、2%丙泊酚组、4%丙泊酚组大鼠干预后第1~4 d水中逃避潜伏期随时间均依次减少(F/P=20.070/0.001,28.440/0.001,18.720/0.001),且4%丙泊酚组>2%丙泊酚组>对照组(F/P=10.725/0.001,13.680/0.001,18.495/0.001,24.120/0.001);穿越平台次数比较,4%丙泊酚组<2%丙泊酚组<对照组(F/P=22.350/0.001)。大鼠血清TNF-α、IL-1β水平比较,4%丙泊酚组>2%丙泊酚组>对照组(F/P=29.745/0.001,34.860/0.001);脑组织P-PI3K、P-Akt表达水平比较,4%丙泊酚组<2%丙泊酚组<对照组(F/P=32.040/0.001,33.285/0.001)。结论丙泊酚麻醉大鼠可致认知功能降低,通过PI3K/Akt通路激活炎性反应,最终导致脑损伤的发生。 Objective To observe the effect of phosphatidylinositol 3-kinase(PI3 K)/protein kinase B(Akt)pathway on brain injury induced by propofol anesthesia in rats.Methods From March 2020 to April 2021,a propofol anesthesia-induced brain injury experiment in rats was conducted at the Central Hospital of Tujia and Miao Autonomous Prefecture,Enshi.Thirty SD rats were selected and randomly divided into control group,2%propofol group and 4%propofol group,each with 10 rats.Rats in the 2%propofol group and the 4%propofol group were given the corresponding concentrations of propofol to establish models,while the control group was only given 1%sodium chloride intramuscular injection for intervention.After continuous intervention for 4 days,the learning and memory ability,serum inflammatory factors[tumor necrosis factor-α(TNF-α),interleukin-1β(IL-1β)],and PI3 K/Akt pathway protein expressions in brain tissue were compared in each group.Results The escape latency in water of rats in the control group,2%propofol group and 4%propofol group decreased with time on the 1 st to 4 th day after intervention(F/P=20.070/0.001,28.440/0.001,18.720/0.001),and the 4%propofol group>2%propofol group>Control group(F/P=10.725/0.001,13.680/0.001,18.495/0.001,24.120/0.001).Comparing the times of crossing the platform,4%propofol group<2%propofol group<control group(F/P=22.350/0.001).Comparison of serum TNF-αand IL-1βlevels in rats,4%propofol group>2%propofol group>control group(F/P=29.745/0.001,34.860/0.001).Compared with the expression of P-PI3 K and PAkt in brain tissue,4%propofol group<2%propofol group<control group(F/P=32.040/0.001,33.285/0.001).Conclusion Propofol anesthetized rats can reduce cognitive function,activate inflammatory response through the PI3 K/Akt pathway,and eventually lead to brain damage.
作者 向思曲 朱贤林 叶刚 王在平 杨敏 Xiang Siqu;Zhu Xianlin;Ye Gang;Wang Zaiping;Yang Min(Department of Anesthesiology,the Central Hospital of Enshi Tujia and Miao Autonomous Prefecture,Hubei Province,Hubei Province,Enshi 445000,China)
出处 《疑难病杂志》 CAS 2022年第3期293-296,共4页 Chinese Journal of Difficult and Complicated Cases
基金 湖北省自然科学基金项目(ZRMS2016001263)。
关键词 丙泊酚 脑损伤 磷脂酰肌醇-3-激酶 蛋白激酶B 麻醉 大鼠 Propofol Brain injury Phosphatidylinositol 3 kinase Protein kinase B Anesthesia Rats
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