| 代娟,张敏.右美托咪定在体外对原代海马神经元氧化应激损伤的影响[J].安徽医药,2021,25(11):2170-2173. |
| 右美托咪定在体外对原代海马神经元氧化应激损伤的影响 |
| Protective effect of dexmedetomidine against oxidative damage of rat hippocampal neurons and it's mechanism |
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| DOI：10.3969/j.issn.1009-6469.2021.11.011 |
| 中文关键词: 右美托咪啶 氧化应激 海马神经元 细胞外信号调节激酶 1/2 脑源性神经营养因子 |
| 英文关键词: Dexmedetomidine Oxidative stress Hippocampal neuron ERK1/2 BNDF |
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| 中文摘要: |
| 目的探讨右美托咪定在体外减弱原代海马神经元的氧化应激损伤的机制。方法将培养的原代海马神经元分为 5组:空白对照组( C组)、损伤对照组( S组)、右美托咪定组( D组)D1，D2，D3组加入不同剂量的右美托咪定( 0.001 μmol/L、0.1 μmol/L、10 μmol/L)。利用 1 mmol/L的过氧化氢( H2O2)处理原代海，马神经元 1h，制作神经元氧化应激损伤模型。按照以上分组情况加入右美托咪定， 37 ℃、5％二氧化碳孵箱孵育 6h。通过测定细胞存活率和上清液中乳酸脱氢酶( LDH)的活性确定减轻海马神经元损伤的右美托咪定的适宜浓度。并检测细胞内丙二醛( MDA)含量、超氧化物歧化酶( SOD)活性的变化。应用逆转录聚合酶链反应( RT-PCR)方法测量各组细胞外信号调节激酶( ERK)1/2和脑源性神经营养因子( BNDF)mRNA表达量。结果右美托咪定组( 0.001 μmol/L、0.1 μmol/L、10 μmol/L)细胞存活率分别为( 72.13±2.45)%、(89.34±2.56)%、(78.40± |
| 英文摘要: |
| Objective To observe the protective efect of dexmedetomidine against oxidative damage of rat hippocampal neurons and discuss its mechanism.Methods The hippocampal neurons were divided into 5 groups:control group, injury group,and 3 different doses of dexmedetomidine groups(0.001 μmol/L,0.1 μmol/L,10 μmol/L).Oxidative stress model was established by incubating hippocampal neurons with H2O2(1 mmol/L)for 1 hour. Different levels of dexmedetomidine were added to oxidative damaged neurons and thenthese neurons were cultured in incubator for 6 hours.To selecte the most fittest concentration of dexmedetomidine by testing viability ofneurons and activity of LDH.Then MDA concentration and SOD activity were (checked) measured.Tae expression of apoptosis factorsincluding ERK1/2 and BNDF was detected by Real—time fluorescent quantitative PCR.Results Cell survival in the dextrotopyrimidine group (0.001 μmol/L, 0.1 μmol/L, 10 μmol/L) was (72.13 ± 2.45)%, (89.34 ± 2.56)%,% (78.40 ± 2.60)%, respectively, all higherthan in the damage group (51.04 ± 2.12)% and were statistically significant (P<0.05).The activity of LDH in dexmedetomidine groups atvaried concentrations(0.001 μmol/L,0.1 μmol/L,10 μmol/L)was significiantly lower than that in H2O2group.It was found that 0.1 μmol/L dexmedetomidine had the furthest protective efect against oxidative damage in primary cultures of rat hippocampal neurons inducedby H2O2.The concentration of MDA and the rate of neuronal apoptosis of dexmedetomidine group(0.1 μmol/L) were much lower than H202 group,while SOD activity was much higher.In dexmedetomidine group(0.1 μmol/L), the expression of ERK1/2 and BNDF was significantly up-regulated .Conclusions Proper dose of dexmedetomidine has remarkable protective efect against oxidative stress in primary cultures of rat hippocampal neurons induced by H202,the mechanism may be related to decreasing the neuronal apoptosis and enhancing the antioxidation of hippocampal neurons.This function maybe related to the ERK1/2 and BNDF pathway. |
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