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七氟醚预处理上调 TIMP3 表达减轻心肌缺血/再灌注损伤。

Precondition of sevoflurane upregulates TIMP3 expression to alleviate myocardial ischemia/reperfusion injury.

机构信息

Department of Cardiovascular Medicine, Affiliated Hospital of Jiangnan University, Wuxi, Jiangsu, China.

Department of Anesthesiology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China.

出版信息

Perfusion. 2021 Oct;36(7):717-723. doi: 10.1177/0267659120960306. Epub 2020 Oct 4.

DOI:10.1177/0267659120960306
PMID:33016228
Abstract

BACKGROUND

Previous studies have pointed out that sevoflurane (Sef) preconditioning could relieve myocardial ischemia/reperfusion (I/R) injury, but the mechanisms is still unknown.

METHODS

C57BL/6 mice model of myocardial I/R injury was established to evaluate the function of Sef. Briefly, Sef was inhaled before I/R operation. The levels of TIMP3, oxidative damage-related factors, and mitogen activated protein kinases (MAPKs) pathway-related factors were measured by qRT-PCR and western blot. Myocardial infarction (MI) area was detected by triphenyl tetrazolium chloride (TTC) staining assay.

RESULTS

Sef preconditioning reduced MI area in myocardial I/R injury mice and upregulated TIMP3 expression in myocardial tissues of I/R mice. In addition, downregulation of TIMP3 reversed the alleviating effects of Sef pretreatment on myocardial oxidative damage and inhibited the effect of Sef pretreatment on MAPKs pathway activity.

CONCLUSION

Sef preconditioning ameliorated myocardial I/R injury by modulating MAPKs pathway activity via upregulating TIMP3.

摘要

背景

先前的研究指出,七氟醚(Sef)预处理可以减轻心肌缺血/再灌注(I/R)损伤,但具体机制尚不清楚。

方法

建立 C57BL/6 小鼠心肌 I/R 损伤模型,以评估 Sef 的功能。简要来说,在 I/R 手术前吸入 Sef。通过 qRT-PCR 和 Western blot 检测 TIMP3、氧化损伤相关因子和丝裂原活化蛋白激酶(MAPKs)途径相关因子的水平。通过氯化三苯基四氮唑(TTC)染色检测心肌梗死(MI)面积。

结果

Sef 预处理可减少心肌 I/R 损伤小鼠的 MI 面积,并上调 I/R 小鼠心肌组织中的 TIMP3 表达。此外,下调 TIMP3 可逆转 Sef 预处理对心肌氧化损伤的缓解作用,并抑制 Sef 预处理对 MAPKs 途径活性的作用。

结论

Sef 预处理通过上调 TIMP3 调节 MAPKs 途径活性,改善心肌 I/R 损伤。

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