右美托咪定对H9C2心肌细胞缺氧/复氧损伤的保护作用(1)
摘 要：目的 观察右美托咪定对H9C2心肌细胞缺氧/复氧损伤的保护作用。方法 H9C2心肌细胞随机分为三组：正常对照组(Control)、缺氧/复氧组(H/R)、Dex(5 μmol/L)干预H/R组。Dex干预H/R组先用Dex预处理6 h后，再经缺氧/复氧处理。采用倒置显微镜观察各组H9C2心肌细胞形态的变化，检测各组细胞培养基中LDH的含量，CCK-8法检测各组H9C2心肌细胞的存活率，试剂盒检测caspase-3活性，TUNEL法检测细胞凋亡并计算凋亡指数。结果 与Control组相比，H/R组细胞皱缩，大量死亡，细胞活力降低，培养基中LDH含量增加，caspase-3活性增加，细胞凋亡指数增加，统计学意义显著(P<0.01)；Dex预处理可明显改善H/R处理后细胞形态，提高细胞活力，减少LDH含量和caspase-3活性，降低细胞凋亡指数，统计学意义显著(P<0.01)。结论 Dex可通过减少H9C2心肌细胞缺氧/复氧引起的细胞凋亡减轻损伤。
关键词：右美托咪定；H9C2；缺氧/復氧；细胞凋亡
, 百拇医药
中图分类号：R917 文献标识码：A DOI：10.3969/j.issn.1006-1959.2018.09.025
文章编号：1006-1959(2018)09-0083-04
Abstract：Objective To observe the protective effects of dexmedetomidine on hypoxia/reoxygenation injury of H9C2 cardiomyocytes. Methods H9C2 cardiomyocytes were randomly divided into three groups： normal control group(Control)，hypoxia/reoxygenation group (H/R)and Dex(5μmol/L)intervention group.Dex intervention in group H/R was treated with Dex pretreatment for 6 h before anoxia/ reoxygenation.The morphologic changes of H9C2 cardiomyocytes in each group were observed by inverted microscope.The content of LDH in the cell culture medium of each group was detected.The survival rate of H9C2 cardiomyocytes in each group was detected by CCK-8 method.The activity of caspase-3 was detected by the kit.The apoptosis was detected by TUNEL method and the apoptosis index was calculated.Results Compared with the Control group，the cells in the H/R group were shrinking，a large number of deaths， the decrease of cell vitality，the increase of LDH content in the medium，the increase of the activity of caspase-3，the increase of the apoptosis index，and the significant statistical significance(P<0.01).Dex pretreatment could obviously improve the morphology of the cells after H/R treatment，raise the vitality of the cells，reduce the content of LDH and caspase-3 activity decreased the apoptotic index，and the difference was statistically significant(P<0.01).Conclusion Dex can reduce the injury of H9C2 cardiomyocytes induced by hypoxia/reoxygenation.
, 百拇医药
Key words：Dexmedetomidine；H9C2；Hypoxia/Reoxygenation；Apoptosis
缺血性心脏病是导致死亡的一类主要的心血管疾病，严重危害人类健康，及时有效的恢复缺血心肌的血流-即再灌注，是临床治疗的首选，然而缺血心肌恢复血流的同时会加重心肌损伤和能量代谢障碍，形成心肌缺血再灌注损伤(myocardial ischemia reperfusion injury， MIRI)[1-3]。右美托咪定(dexmedetomidine， Dex)是一种新型的高选择性α2受体激动剂，被广泛应用于心血管手术的麻醉，并收到了较好的效果。Dex在心血管疾病中发挥保护作用，但具体机制仍不清楚。Dex具有剂量依赖性的镇静、镇痛、抗焦虑和抑制交感神经兴奋等作用，且对呼吸、循环的抑制作用轻微[8-10]。Dex对心肌的保护作用受到越来越多的关注，普遍认为Dex是通过抑制交感中枢活动，降低心率，降低心肌氧耗，改善心肌氧供需平衡，但具体机制仍未阐明。本研究采用H9C2心肌细胞缺氧/复氧模型，观察Dex预处理对缺氧/复氧损伤的影响及其可能机制，现分析如下。, http://www.100md.com(李璟 蒋娜 王晶晶 马兴建 王家宾)
关键词：右美托咪定；H9C2；缺氧/復氧；细胞凋亡
, 百拇医药
中图分类号：R917 文献标识码：A DOI：10.3969/j.issn.1006-1959.2018.09.025
文章编号：1006-1959(2018)09-0083-04
Abstract：Objective To observe the protective effects of dexmedetomidine on hypoxia/reoxygenation injury of H9C2 cardiomyocytes. Methods H9C2 cardiomyocytes were randomly divided into three groups： normal control group(Control)，hypoxia/reoxygenation group (H/R)and Dex(5μmol/L)intervention group.Dex intervention in group H/R was treated with Dex pretreatment for 6 h before anoxia/ reoxygenation.The morphologic changes of H9C2 cardiomyocytes in each group were observed by inverted microscope.The content of LDH in the cell culture medium of each group was detected.The survival rate of H9C2 cardiomyocytes in each group was detected by CCK-8 method.The activity of caspase-3 was detected by the kit.The apoptosis was detected by TUNEL method and the apoptosis index was calculated.Results Compared with the Control group，the cells in the H/R group were shrinking，a large number of deaths， the decrease of cell vitality，the increase of LDH content in the medium，the increase of the activity of caspase-3，the increase of the apoptosis index，and the significant statistical significance(P<0.01).Dex pretreatment could obviously improve the morphology of the cells after H/R treatment，raise the vitality of the cells，reduce the content of LDH and caspase-3 activity decreased the apoptotic index，and the difference was statistically significant(P<0.01).Conclusion Dex can reduce the injury of H9C2 cardiomyocytes induced by hypoxia/reoxygenation.
, 百拇医药
Key words：Dexmedetomidine；H9C2；Hypoxia/Reoxygenation；Apoptosis
缺血性心脏病是导致死亡的一类主要的心血管疾病，严重危害人类健康，及时有效的恢复缺血心肌的血流-即再灌注，是临床治疗的首选，然而缺血心肌恢复血流的同时会加重心肌损伤和能量代谢障碍，形成心肌缺血再灌注损伤(myocardial ischemia reperfusion injury， MIRI)[1-3]。右美托咪定(dexmedetomidine， Dex)是一种新型的高选择性α2受体激动剂，被广泛应用于心血管手术的麻醉，并收到了较好的效果。Dex在心血管疾病中发挥保护作用，但具体机制仍不清楚。Dex具有剂量依赖性的镇静、镇痛、抗焦虑和抑制交感神经兴奋等作用，且对呼吸、循环的抑制作用轻微[8-10]。Dex对心肌的保护作用受到越来越多的关注，普遍认为Dex是通过抑制交感中枢活动，降低心率，降低心肌氧耗，改善心肌氧供需平衡，但具体机制仍未阐明。本研究采用H9C2心肌细胞缺氧/复氧模型，观察Dex预处理对缺氧/复氧损伤的影响及其可能机制，现分析如下。, http://www.100md.com(李璟 蒋娜 王晶晶 马兴建 王家宾)