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丙泊酚对氯化钴诱导人心肌AC16细胞低氧损伤的保护作用 被引量:6

Propofol protects human cardiac AC16 cells from CoCl_2-induced hypoxic injury
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摘要 目的:研究丙泊酚预处理对氯化钴(cobalt chloride,CoCl2)诱导离体人心肌AC16细胞低氧损伤的影响及其相关的分子机制。方法:以CoCl2处理的人心肌AC16细胞作为心肌细胞低氧的体外模型。将AC16细胞分为对照组、CoCl2诱导低氧组(CoCl2组)和丙泊酚+CoCl2诱导低氧组(Propofol+CoCl2组)。采用细胞计数试剂盒-8(cell counting kit-8,CCK-8)评估细胞活力;采用流式细胞术分析AC16细胞凋亡比率(apoptosis ratio,AR)和线粒体膜电位(mitochondrial membrane potential,Δψm);采用对线粒体活性氧(reactive oxygen species,ROS)敏感的荧光探针测定各组AC16细胞中ROS含量,并检测AC16细胞中的丙二醛(malondialdehyde,MDA)和超氧化物歧化酶(superoxide dismutase,SOD)水平;采用Western印迹评估c-Jun氨基末端激酶(c-Jun N-terminal kinase,JNK)和p38信号转导途径的激活。结果:1)与对照组相比,以500μmol/L CoCl2处理12 h的CoCl2组AC16细胞活力显著降低(P<0.01);2)与对照组相比,CoCl2组和Propofol+CoCl2组AC16细胞的AR均显著升高,而Δψm均显著降低(均P<0.01);与CoCl2组相比,Propofol+CoCl2组AC16细胞的AR显著降低,而Δψm显著升高(均P<0.05);3)与对照组相比,CoCl2组的ROS和MDA水平显著升高,SOD水平显著降低(均P<0.01);与对照组相比,Propofol+CoCl2组ROS和MDA水平显著升高,SOD水平显著降低(均P<0.05);4)与对照组相比,CoCl2组JNK和p38的磷酸化水平显著升高(均P<0.05);与CoCl2组相比,Propofol+CoCl2组JNK和p38的磷酸化水平显著降低(均P<0.05)。结论:丙泊酚预处理可能通过抑制JNK和p38信号通路的激活,从而保护人心肌AC16细胞免受CoCl2诱导的低氧损伤。 Objective:To explore the effect of propofol on human cardiac AC16 cells under CoCl2-induced hypoxic injury and the possible mechanisms.Methods:Human AC16 cardiomyocytes were treated with cobalt chloride(CoCl2)to mimic hypoxic condition in cultured cardiomyocytes.The AC16 cells were divided into 3 groups:a control group,a CoCl2 hypoxia group(CoCl2 group),and a propofol+CoCl2 group(propofol+CoCl2 group).The cell viability was assessed by cell counting kit-8(CCK-8).Cell apoptosis ratio(AR)and the mitochondrial membrane potential(Δψm)were detected by flow cytometry.The reactive oxygen species(ROS)production in AC16 cells were determined with the ROS-sensitive fluorescent probe.Meanwhile,total intracellular levels of malondialdehyde(MDA)and superoxide dismutase(SOD)in AC16 cells were detected with commercially available kits.Western blot was used to evaluate the activation of c-Jun N-terminal kinase(JNK)and p38 signaling pathways.Results:1)Compared with the control group,AC16 cell viability was decreased significantly in the CoCl2 group following the treatment with 500μmol/L CoCl2(P<0.01);2)Compared with the control group,AR value in AC16 cells was increased significantly in the CoCl2 group,whileΔψm was decreased significantly(all P<0.01).Compared with the CoCl2 group,AR value in AC16 cells was decreased significantly in the propofol+CoCl2 group,whileΔψm was increased significantly(both P<0.05);3)Compared with the control group,the levels of ROS and MDA were increased significantly,and the level of SOD was significantly decreased in the CoCl2 group(all P<0.01).Compared with the CoCl2 group,the ROS and MDA levels in the propofol+CoCl2 group were increased significantly and the SOD levels were decreased significantly(all P<0.05);4)Compared with the control group,the phosphorylation levels of JNK and p38 were increased significantly(both P<0.05)in the CoCl2 group.Compared with the CoCl2 group,the phosphorylation levels of JNK and p38 were decreased significantly in the propofol+CoCl2 group(both P<0.05).Conclusion:The pretreatment with propofol may protect human cardiac AC16 cells from the chemical hypoxia-induced injury through regulation of JNK and p38 signaling pathways.
作者 韩流 章晓丹 钱燕宁 HAN Liu;ZHANG Xiaodan;QIAN Yanning(Department of Anesthesiology,First Affiliated Hospital,Nanjing Medical University,Nanjing 210029;Department of Anesthesiology,Nanjing Hospital Affiliated to Nanjing Medical University(Nanjing First Hospital),Nanjing 210006,China)
出处 《中南大学学报(医学版)》 CAS CSCD 北大核心 2019年第3期307-314,共8页 Journal of Central South University :Medical Science
基金 国家自然科学基金(81671387)~~
关键词 丙泊酚 心肌细胞 低氧 凋亡 C-JUN氨基末端激酶 P38 propofol cardiomyocyte hypoxia apoptosis c-Jun N-terminal kinase p38
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