摘要
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Fe^(2+)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·mL^(-1),Fe^(2+)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。
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 and10μmo L·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 Fe^(2+)levels were detected by Ferro Orange 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) m U·m L^(-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·m L^(-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·m L^(-1),respectively;Fe^(2+)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.
作者
董伟
王娟
赵伟
贲晨
DONG Wei;WANG Juan;ZHAO Wei;BEN Chen(Anesthesia Department,Huaibei Miner General Hospital,Huaibei 235000,Anhui Province,China;Cardiothoracic Surgery Department,Huaibei Miner General Hospital,Huaibei 235000,Anhui Province,China)
出处
《中国临床药理学杂志》
CAS
CSCD
北大核心
2024年第3期354-357,共4页
The Chinese Journal of Clinical Pharmacology
关键词
右美托咪定
铁代谢
氧糖剥夺/再灌注
心肌细胞
氧化应激
dexmedetomidine
iron metabolism
oxygen-glucose deprivation/reperfusion
cardiomyocytes
oxidative stress
