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大蒜素可能通过调节 JAK2/STAT3 通路抑制血管内皮细胞的活性。

Allicin can suppress the activity of vascular endothelial cells probably by regulating JAK2/STAT3 pathway.

机构信息

Department of Orthopedics, Clinical Medical College, Yangzhou University, Yangzhou, Jiangsu, China.

Department of Spinal Surgery, Department of Orthopedics, Clinical Medical College, Yangzhou University, Yangzhou, 225001, Jiangsu, China.

出版信息

Mol Cell Biochem. 2021 Jan;476(1):435-441. doi: 10.1007/s11010-020-03919-z. Epub 2020 Sep 25.

DOI:10.1007/s11010-020-03919-z
PMID:32975696
Abstract

Whether allicin can suppress the angiogenesis via inhibiting the activity of vascular endothelial cells (VECs) in preventing epidural hypertrophic scars remains unknown. VECs were treated by allicin at a gradient of concentrations. Cell activity was measured by CCK-8 assay, scratch assay and flow cytometry. Reverse-transcription PCR and Western Blot were used to measure the expression levels of relevant genes and proteins. After treated with allicin at concentrations of 0, 25, 50 and 100 mg/L, the viability of VECs significantly decreased at 24 h (p < 0.001*) and 48 h (p < 0.001*), and migration rate significantly decreased in scratch assay (p = 0.017*) and in Transwell assay (p = 0.021*). As the concentrations of allicin increased, the apoptosis rate of VECs rose up (p = 0.018*). There was no significant difference on cell numbers at S phase (p = 0.25), but cell numbers at G1 phase decreased (p = 0.039*) and at G2 phase increased (p = 0.047*). With the increase of allicin concentrations, the ability of tube formation for VECs significantly decreased (p < 0.001*). Comparing with control group, the expression of PCNA and BCL-2 decreased (p < 0.001*), while the expression of BAX increased significantly (p < 0.001*). Regarding to JAK2/STAT3 pathway, the expression levels of JAK3 and STAT3 decreased significantly with the increase of allicin concentrations (p < 0.001*). Allicin can suppress the activity of VECs probably by regulating JAK2/STAT3 pathway.

摘要

大蒜素是否可以通过抑制血管内皮细胞 (VECs) 的活性来抑制血管生成,从而预防硬膜外肥厚性瘢痕,目前尚不清楚。用大蒜素梯度浓度处理 VECs。通过 CCK-8 测定法、划痕试验和流式细胞术测定细胞活性。使用逆转录 PCR 和 Western Blot 测定相关基因和蛋白的表达水平。用浓度为 0、25、50 和 100 mg/L 的大蒜素处理后,VECs 的活力在 24 小时(p<0.001*)和 48 小时(p<0.001*)显著降低,划痕试验(p=0.017*)和 Transwell 试验(p=0.021*)中迁移率显著降低。随着大蒜素浓度的增加,VECs 的凋亡率上升(p=0.018*)。S 期细胞数量无显著差异(p=0.25),但 G1 期细胞数量减少(p=0.039*),G2 期细胞数量增加(p=0.047*)。随着大蒜素浓度的增加,VECs 的管形成能力显著降低(p<0.001*)。与对照组相比,PCNA 和 BCL-2 的表达降低(p<0.001*),而 BAX 的表达显著增加(p<0.001*)。关于 JAK2/STAT3 通路,随着大蒜素浓度的增加,JAK3 和 STAT3 的表达水平显著降低(p<0.001*)。大蒜素可能通过调节 JAK2/STAT3 通路来抑制 VECs 的活性。

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