首页|右美托咪定调控铁代谢对氧糖剥夺/再灌注心肌细胞损伤的保护作用

右美托咪定调控铁代谢对氧糖剥夺/再灌注心肌细胞损伤的保护作用

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目的 探究右美托咪定调控铁代谢对氧糖剥夺/再灌注(OGD/R)心肌细胞损伤的影响.方法 体外培养H9c2心肌细胞,分为对照组(常规培养)、模型组(OGD/R处理)和低、中、高剂量实验组(氧糖剥夺/再灌注后用1、5和10μmoL·L-1右美托咪定处理).用流式细胞术检测细胞凋亡,用酶联免疫吸附试验法检测谷胱甘肽过氧化物酶(GSH-PX)、超氧化物歧化酶(SOD)、乳酸脱氢酶(LDH)水平,用FerroOrange荧光探针检测Fe2+水平.结果 对照组、模型组和低、中、高剂量实验组的凋亡率分别为(4.11±0.35)%、(27.57±2.36)%、(20.52±1.43)%、(14.17±1.55)%和(8.47±0.89)%,GSH-PX 分别 为(26.75±3.14)、(126.68±11.42)、(98.74±9.23)、(73.15±8.02)和(45.85±4.80)mU·mL-1,SOD 分别为(1.59±0.11)、(7.52±1.13)、(6.12±0.74)、(4.97±0.54)和(2.35±0.69)ng·mL-1,LDH 分别为(13.42±1.53)、(152.15±18.94)、(103.15±12.45)、(64.59±7.81)和(27.85±3.42)ng·mL1,Fe2+水平分别为(20.26±2.93)、(63.85±6.44)、(52.17±4.58)、(40.15±4.12)和(27.48±3.08)mmol·L-1.对照组的上述指标与模型组比较,在统计学上差异均有统计学意义(均P<0.05);模型组的上述指标与低、中、高剂量实验组比较,在统计学上差异均有统计学意义(均P<0.05).结论 右美托咪定可通过调控铁代谢减轻OGD/R所致的心肌细胞损伤.
Protective effects of dexmedetomidine on oxygen glucose deprivation/reperfusion cardiomyocyte injury by regulating iron metabolism
Objective To investigate the effect of dexmedetomide on oxygen glucose deprivation/reperfusion(OGD/R)myocardial cell injury.Methods H9c2 cardiomyocytes were cultured in vitro and divided into control group(routine culture),model group(OGD/R treatment),experimental-L,-M,-H groups(treated with 1,5 and 10 μmoL·L-1 dexmedetomidine after oxygen glucose deprivation/reperfusion).Apoptosis was detected by flow cytometry;the levels of glutathione peroxidase(GSH-PX),superoxide dismutase(SOD)and lactate dehydrogenase(LDH)were detected by enzyme-linked immunosorbent assay;and Fe2+levels were detected by FerroOrange fluorescent probe.Results The apoptosis rates of control group,model group,experimental-L,-M,-H groups were(4.11±0.35)%,(27.57±2.36)%,(20.52±1.43)%,(14.17±1.55)%,(8.47±0.89)%,respectively;GSH-PX were(26.75±3.14),(126.68±11.42),(98.74±9.23),(73.15±8.02),(45.85±4.80)mU·mL-1,respectively;SOD were(1.59±0.11),(7.52±1.13),(6.12±0.74),(4.97±0.54),(2.35±0.69)ng·mL-1,respectively;LDH were(13.42±1.53),(152.15±18.94),(103.15±12.45),(64.59±7.81),(27.85±3.42)ng·mL-1,respectively;Fe2+were level(20.26±2.93),(63.85±6.44),(52.17±4.58),(40.15±4.12),(27.48±3.08)mmol·L-1,respectively.There were statistically significant differences between control group and model group(all P<0.05);the model group was compared with experimental-L,-M,-H groups,and the differences were statistically significant(all P<0.05).Conclusion Dexmedetomidine can alleviate myocardial cell injury induced by OGD/R by regulating iron metabolism.

dexmedetomidineiron metabolismoxygen-glucose deprivation/reperfusioncardiomyocytesoxidative stress

董伟、王娟、赵伟、贲晨

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淮北矿工总医院麻醉科,安徽淮北 235000

淮北矿工总医院心胸外科,安徽淮北 235000

右美托咪定 铁代谢 氧糖剥夺/再灌注 心肌细胞 氧化应激

2024

中国临床药理学杂志
中国药学会

中国临床药理学杂志

CSTPCD北大核心
影响因子:1.91
ISSN:1001-6821
年,卷(期):2024.40(3)
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