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5′-N-乙基酰胺基腺苷对大鼠脑缺血再灌注氧化损伤和脑组织miR-29b、miR-125b水平的影响

Effects of 5′-N-ethylocarbo-xamidoad-enosine on brain ischemia-reperfusion oxidative injury and levels of miR-29b and miR-125b in rats
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摘要 目的探究5′-N-乙基酰胺基腺苷(NECA)对大鼠脑缺血再灌注氧化损伤和脑组织中miR-29b、miR-125b水平的影响。方法将SD大鼠随机分为假手术组、模型组、实验组和阳性对照组,每组12只。建模前7 d,实验组腹腔注射1.5 mg·kg^(-1)的NECA;阳性对照组腹腔注射2.0 mg·kg^(-1)的尼莫地平;假手术组和模型组均腹腔注射等量0.9%NaCl。4组大鼠每天给药1次,连续给药7 d。除假手术组外,其余3组均用大脑中动脉栓塞方法建立脑缺血再灌注模型。建模成功后,用酶联免疫吸附试验法测定大鼠血清氧化应激指标[谷胱甘肽(GSH)、超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、丙二醛(MDA)]水平,用实时荧光定量聚合酶链反应法检测脑组织中miR-29b、miR-125b的表达水平。结果假手术组、模型组、实验组和阳性对照组的SOD分别为(57.82±6.87)、(10.75±0.24)、(32.24±3.42)和(29.45±4.11)U·mL^(-1),GSH分别为(20.62±3.12)、(9.45±1.92)、(16.78±1.85)和(15.39±2.02)U·mg^(-1),CAT分别为(3.25±0.42)、(0.85±0.11)、(2.18±0.34)和(1.98±0.32)U·L^(-1),MDA分别为(0.42±0.09)、(1.35±0.42)、(0.75±0.06)和(0.72±0.08)nmol·mg^(-1),脑组织中miR-29b表达水平分别为1.02±0.11、0.42±0.02、0.84±0.08和0.87±0.10,miR-125b表达水平分别为1.00±0.11、0.48±0.05、0.75±0.08和0.74±0.07。模型组的上述指标与实验组、阳性对照组和假手术组比较,在统计学上差异均有统计学意义(均P<0.05)。结论NECA可改善脑缺血再灌注大鼠氧化损伤,并增加miR-29b和miR-125b水平。 Objective To investigate the effects of′-N-ethylocarbo-xamidoad-enosine(NECA)on cerebral ischemia-reperfusion oxidative injury and the levels of miR-29b and miR-125b in rats.Methods SD rats were divided into sham-operation,model,experimental and positive control groups with 12 rats in each group.Cerebral ischemia-reperfusion model was established in all the other 3 groups except control group.7 days before modeling,sham-operation group and model group were intraperitoneally injected with the same amount of normal saline,and experimental group was injected with 1.5 mg·kg^(-1)NECA,and positive control group was injected with 2.0 mg·kg^(-1)nimodipine.The rats in 4 groups were given the drug once a day for 7 days.Cerebral ischemia-reperfusion model was established by middle cerebral artery embolization in all the other 3 groups except sham-operation group.After the modeling was successful,the serum oxidative stress indexes glutathione(GSH),superoxide dismutase(SOD),catalase(CAT),malondialdehyde(MDA)of rats were determined by enzyme-linked immunosorbent assay,and the levels of miR-29b and miR-125b in brain tissue were detected by real-time fluorescence quantitative polymerase chain reaction.Results The SOD levels of sham-operation,model,experimental and positive control groups were(57.82±6.87),(10.75±0.24),(32.24±3.42)and(29.45±4.11)U·mL^(-1);the levels of GSH were(20.62±3.12),(9.45±1.92),(16.78±1.85)and(15.39±2.02)U·mg^(-1);the levels of CAT were(3.25±0.42),(0.85±0.11),(2.18±0.34)and(1.98±0.32)U·L^(-1);the levels of MDA were(0.42±0.09),(1.35±0.42),(0.75±0.06)and(0.72±0.08)nmol·mg^(-1);the expression levels of miR-296 in brain tissue were 1.02±0.11,0.42±0.02,0.84±0.08 and 0.87±0.10;the expression levels of miR-125b in brain tissue were 1.00±0.11,0.48±0.05,0.75±0.08 and 0.74±0.07,respectively.There were statistically significant differences between sham-operation group and model group(all P<0.05).Compared with experimental group and positive control group,there were statistically significant differences in the above indexes(all P<0.05).Conclusionn NECA can improve oxidative damage and increase the expression levels of miR-29b and miR-125b in cerebral ischemia-reperfusion rats.
作者 李泽 谭军 明秋丽 栗延伟 LI Ze;TAN Jun;MING Qiu-li;LI Yan-wei(Department of Neurology,The Third Affiliated Hospital of Xinxiang Medical College,Xinxiang 453000,Henan Province,China)
出处 《中国临床药理学杂志》 CAS CSCD 北大核心 2024年第10期1448-1452,共5页 The Chinese Journal of Clinical Pharmacology
基金 河南省医学科技攻关计划联合共建立项基金资助项目(LIIGJ20200533)。
关键词 5′-N-乙基酰胺基腺苷 脑缺血再灌注 氧化损伤 脑组织 微小RNA-29b 微小RNA-125b adenosine receptor agonist cerebral ischemia reperfusion oxidative damage brain tissue microRNA-29b microRNA-125b
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