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薰衣草通过靶向JAK2/STAT3信号通路保护H9c2心肌细胞免受氧糖剥夺（OGD）诱导的损伤。

Lavender protects H9c2 cardiomyocytes against oxygen-glucose deprivation (OGD)-induced injury via targeting the JAK2/STAT3 pathway.

作者信息

Askarian-Amiri Shaghayegh, Fotovat Eskandari Hoda, Ramezani Fatemeh, Vahabzadeh Gelare, Aboutaleb Nahid

机构信息

Institut de Biologie Structurale (IBS), Univ. Grenoble Alpes, CEA, CNRS, 71 Avenue des Martyrs, 38000 Grenoble, France.

Physiology Research Center, Iran University of Medical Sciences, Tehran, Iran.

出版信息

Iran J Basic Med Sci. 2022 Feb;25(2):263-267. doi: 10.22038/IJBMS.2022.54751.12280.

DOI:10.22038/IJBMS.2022.54751.12280
PMID:35655588
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9124541/
Abstract

OBJECTIVES

This study was conducted to examine the therapeutic effects of lavender oil (LO) against oxygen-glucose deprivation (OGD)-induced injury model.

MATERIALS AND METHODS

In this study, the OGD model was induced in the H9C2 cell line, and then the cells were treated with LO (10, 100, 1000, and 10000 μg/ml). The anti-inflammatory activity of LO (JAK2/STAT3) was evaluated by immunocytochemical assay. Likewise, the p-ERK/ERK level was measured by western blotting.

RESULTS

Compared with only the OGD-induced injury model, cell survival increased after treatment with LO. Our results showed that 100 μg/ml of LO significantly decreased the expression of Jak2/Stat3 and the apoptotic activity 72 hr after reperfusion compared with the control group. Likewise, significant increases were observed in p-ERK/ERK in LO-treated groups.

CONCLUSION

Collectively, these findings confirm that LO can be a good candidate to reduce OGD-induced injury in the H9C2 cell line through targeting Jak2/Stat3 and ERK pathways.

摘要

目的

本研究旨在探讨薰衣草油（LO）对氧糖剥夺（OGD）诱导损伤模型的治疗作用。

材料与方法

本研究在H9C2细胞系中诱导建立OGD模型，然后用LO（10、100、1000和10000μg/ml）处理细胞。通过免疫细胞化学分析评估LO（JAK2/STAT3）的抗炎活性。同样，通过蛋白质印迹法测量p-ERK/ERK水平。

结果

与仅OGD诱导损伤模型相比，用LO处理后细胞存活率增加。我们的结果表明，与对照组相比，100μg/ml的LO在再灌注72小时后显著降低Jak2/Stat3的表达和凋亡活性。同样，在LO处理组中观察到p-ERK/ERK显著增加。

结论

总体而言，这些发现证实LO可以通过靶向Jak2/Stat3和ERK途径成为减轻H9C2细胞系中OGD诱导损伤的良好候选物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f358/9124541/e44ee5b3a548/IJBMS-25-263-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f358/9124541/9e014972682e/IJBMS-25-263-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f358/9124541/722fff54e23e/IJBMS-25-263-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f358/9124541/9c6aed1466e5/IJBMS-25-263-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f358/9124541/e44ee5b3a548/IJBMS-25-263-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f358/9124541/9e014972682e/IJBMS-25-263-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f358/9124541/722fff54e23e/IJBMS-25-263-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f358/9124541/9c6aed1466e5/IJBMS-25-263-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f358/9124541/e44ee5b3a548/IJBMS-25-263-g004.jpg

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