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艾氯胺酮通过调节瞬时受体电位香草酸亚型1（TRPV1）的表达并抑制细胞内钙离子浓度来减轻心肌细胞的缺氧/复氧损伤。

Esketamine alleviates hypoxia/reoxygenation injury of cardiomyocytes by regulating TRPV1 expression and inhibiting intracellular Ca concentration.

作者信息

Zhang Ying, Lu QuanMei, Hu HanChun, Yang ChunChen, Zhao QiHong

机构信息

Department of Anesthesiology, The First Affiliated Hospital of Bengbu Medical College, Bengbu City, Anhui Province, China.

Department of Anesthesiology, The Second Affiliated Hospital of Bengbu Medical College, Bengbu City, Anhui Province, China.

出版信息

Clinics (Sao Paulo). 2024 Apr 30;79:100363. doi: 10.1016/j.clinsp.2024.100363. eCollection 2024.

DOI:10.1016/j.clinsp.2024.100363
PMID:38692008
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11070684/
Abstract

OBJECTIVE

This study aimed to investigate the effect of Esketamine (ESK) on the Hypoxia/Reoxygenation (H/R) injury of cardiomyocytes by regulating TRPV1 and inhibiting the concentration of intracellular Ca.

METHODS

The H/R injury model of H9c2 cardiomyocytes was established after 4h hypoxia and 6h reoxygenation. H9c2 cells were treated with different concentrations of ESK or TRPV1 agonist capsaicin (10 μM) or TRPV1 inhibitor capsazepine (1 μM). Cell viability was detected by CCK-8 method, and apoptosis by flow cytometry. Intracellular Ca concentration was evaluated by Fluo-4 AM. LDH, MDA, SOD, and GSH-Px were detected with corresponding commercial kits. TRPV1 and p-TRPV1 proteins were detected by Western blot.

RESULTS

After H/R, H9c2 cell viability decreased, apoptosis increased, intracellular Ca concentration increased, LDH and MDA levels increased, SOD and GSH-Px levels decreased, and p-TRPV1 expression increased. ESK treatment rescued these changes induced by H/R. After up-regulating TRPV1, the protective effect of ESK on H/R injury of H9c2 cells was weakened, while down-regulating TRPV1 could further protect against H/R injury.

CONCLUSION

ESK alleviates H/R injury of cardiomyocytes by regulating TRPV1 expression and inhibiting intracellular Ca concentration.

摘要

目的

本研究旨在探讨艾司氯胺酮（ESK）通过调节瞬时受体电位香草酸亚型1（TRPV1）和抑制细胞内钙离子浓度对心肌细胞缺氧/复氧（H/R）损伤的影响。

方法

在缺氧4小时和复氧6小时后建立H9c2心肌细胞的H/R损伤模型。用不同浓度的ESK或TRPV1激动剂辣椒素（10μM）或TRPV1抑制剂capsazepine（1μM）处理H9c2细胞。采用CCK-8法检测细胞活力，流式细胞术检测细胞凋亡。用Fluo-4 AM评估细胞内钙离子浓度。用相应的商业试剂盒检测乳酸脱氢酶（LDH）、丙二醛（MDA）、超氧化物歧化酶（SOD）和谷胱甘肽过氧化物酶（GSH-Px）。通过蛋白质免疫印迹法检测TRPV1和磷酸化TRPV1蛋白。

结果

H/R后，H9c2细胞活力下降，凋亡增加，细胞内钙离子浓度增加，LDH和MDA水平升高，SOD和GSH-Px水平降低，磷酸化TRPV1表达增加。ESK处理可挽救H/R诱导的这些变化。上调TRPV1后，ESK对H9c2细胞H/R损伤的保护作用减弱，而下调TRPV1可进一步预防H/R损伤。

结论

ESK通过调节TRPV1表达和抑制细胞内钙离子浓度减轻心肌细胞的H/R损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6575/11070684/f7562f4c8287/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6575/11070684/b6d19a055082/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6575/11070684/3297a5a75ed2/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6575/11070684/9ffbddcef51b/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6575/11070684/de5313f42671/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6575/11070684/f7562f4c8287/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6575/11070684/b6d19a055082/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6575/11070684/3297a5a75ed2/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6575/11070684/9ffbddcef51b/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6575/11070684/de5313f42671/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6575/11070684/f7562f4c8287/gr5.jpg

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