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大蒜素通过抑制 Ca 超载诱导的心肌细胞凋亡，经由 PI3K/GRK2/PLC-γ/IP3R 信号通路对心肌缺血再灌注起到保护作用。

The protective effect of allicin on myocardial ischemia-reperfusion by inhibition of Ca overload-induced cardiomyocyte apoptosis via the PI3K/GRK2/PLC-γ/IP3R signaling pathway.

机构信息

Graduate School of Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing 100730, China.

Department of Integrative Medicine Cardiology, China-Japan Friendship Hospital, Beijing 100029, China.

出版信息

Aging (Albany NY). 2021 Aug 3;13(15):19643-19656. doi: 10.18632/aging.203375.

DOI:10.18632/aging.203375
PMID:34343971
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8386544/
Abstract

PURPOSE

To investigate the protective effect and mechanism of allicin on myocardial ischemia-reperfusion (MI/R) injury.

METHODS

We investigated the mechanisms by which allicin attenuated the MI/R injury by focusing on phosphoinositide 3-kinase, G protein coupled receptor kinases 2, phospholipase Cγ and cardiomyocyte apoptosis. Sixty male mice were randomly assigned into three groups: repeated MI/R (model), sham-operated (control), and MI/R+ allicin group (allicin). Ultrasound examination was used to examine the cardiac function. Masson staining was used to evaluate the myocardial infarct area. TUNEL assay was performed to examine the anti-apoptotic effect of allicin. Differentially expressed genes (DEGs) and pathways were analyzed by mRNA microarray analysis. Immunofluorescence staining and western blot were carried out to detect the effect of allicin on the PI3K. A pan-PLC activator, m-3M3FBS, was applied to investigate whether allicin induced cardiomyocyte apoptosis was via the GRK2/PLC/IP3R signaling pathway.

RESULTS

Masson staining and the TUNEL assay revealed that allicin reduced infarct size and played an anti-apoptotic role in M/IR. Ultrasound examination revealed that allicin improved cardiac function after M/IR injury. Gene ontology analysis indicated that the calcium signaling pathway and PI3KCA(PI3K) were selected. Immunofluorescence staining and western blot exposed that PI3K was activated by allicin during MI/R injury. Fura-2AM staining revealed that the PI3K -mediated GRK2/PLC-γ/IP3R pathway may be involved in the protective effect of allicin on MI/R injury.

CONCLUSIONS

Allicin has a protective effect on MI/R injury. This effect might be associated with the inhibition of Ca overload-induced apoptosis and the inhibition of the PI3K -mediated GRK2/PLC-γ/IP3R signaling pathway.

摘要

目的

研究大蒜素对心肌缺血再灌注（MI/R）损伤的保护作用及其机制。

方法

通过聚焦于磷酸肌醇 3-激酶（PI3K）、G 蛋白偶联受体激酶 2（GRK2）、磷脂酶 Cγ（PLCγ）和心肌细胞凋亡，研究大蒜素减轻 MI/R 损伤的机制。将 60 只雄性小鼠随机分为三组：重复 MI/R（模型）、假手术（对照）和 MI/R+大蒜素组（大蒜素）。超声检查用于检测心功能。Masson 染色用于评估心肌梗死面积。TUNEL 检测用于检测大蒜素的抗凋亡作用。通过 mRNA 微阵列分析分析差异表达基因（DEGs）和途径。免疫荧光染色和 Western blot 用于检测大蒜素对 PI3K 的影响。应用全 PLC 激活剂 m-3M3FBS 研究大蒜素诱导的心肌细胞凋亡是否通过 GRK2/PLC/IP3R 信号通路。

结果

Masson 染色和 TUNEL 检测显示，大蒜素减少了梗死面积并在 MI/R 中发挥抗凋亡作用。超声检查显示，大蒜素改善了 MI/R 损伤后的心脏功能。基因本体分析表明，钙信号通路和 PI3KCA（PI3K）被选择。免疫荧光染色和 Western blot 显示，在 MI/R 损伤过程中，大蒜素激活了 PI3K。Fura-2AM 染色显示，PI3K 介导的 GRK2/PLC-γ/IP3R 通路可能参与了大蒜素对 MI/R 损伤的保护作用。

结论

大蒜素对 MI/R 损伤具有保护作用。这种作用可能与抑制 Ca 超载诱导的细胞凋亡和抑制 PI3K 介导的 GRK2/PLC-γ/IP3R 信号通路有关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb0f/8386544/6d47032dd8bc/aging-13-203375-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb0f/8386544/b549caf39bca/aging-13-203375-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb0f/8386544/ca98d1ef3d09/aging-13-203375-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb0f/8386544/7df591dc29bb/aging-13-203375-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb0f/8386544/2d275afc367f/aging-13-203375-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb0f/8386544/f8121675a15d/aging-13-203375-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb0f/8386544/e07205ddc996/aging-13-203375-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb0f/8386544/6d47032dd8bc/aging-13-203375-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb0f/8386544/b549caf39bca/aging-13-203375-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb0f/8386544/ca98d1ef3d09/aging-13-203375-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb0f/8386544/7df591dc29bb/aging-13-203375-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb0f/8386544/2d275afc367f/aging-13-203375-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb0f/8386544/f8121675a15d/aging-13-203375-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb0f/8386544/e07205ddc996/aging-13-203375-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb0f/8386544/6d47032dd8bc/aging-13-203375-g007.jpg

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