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白花芍药苷通过抑制PARP1/NF-κB信号通路减轻高糖诱导的内皮细胞凋亡。

Albiflorin attenuates high glucose-induced endothelial apoptosis via suppressing PARP1/NF-κB signaling pathway.

作者信息

Yang Rong, Yang Yang

机构信息

Department of Rheumatology and Immunology, Zhongda Hospital Affiliated to Southeast University, Nanjing, 210009, Jiangsu, People's Republic of China.

Department of Cardiology, The First Affiliated Hospital of Nanjing Medical University, 300 Guangzhou Road, Nanjing, 210029, Jiangsu, People's Republic of China.

出版信息

Inflamm Res. 2023 Jan;72(1):159-169. doi: 10.1007/s00011-022-01666-z. Epub 2022 Nov 10.

Abstract

OBJECTIVE

Paeonia lactiflora Pall has long been recognized as an anti-inflammatory traditional Chinese herbal medicine. We aimed to study the pharmacological action of albiflorin, an active ingredient extracted from the roots of Paeonia lactiflora Pall, on diabetic vascular complications.

METHODS

Human umbilical vein endothelial cells (HUVECs) were stimulated with high glucose and treated with 5, 10, and 20 μM albiflorin. CCK-8 assay, EdU staining, Annexin V-FITC staining, transwell assay, scratch test, RT-PCR, ELISA, Western blot, and immunofluorescence were carried out. SwissTargetPrediction database was used for screening targets of albiflorin and molecular docking was done using Autodock Vina software.

RESULTS

Albiflorin treatment dose-dependently alleviated high glucose-induced viability loss of HUVECs. In addition, albiflorin promoted the proliferation and migration, while inhibited apoptosis and the release of TNF-α, IL-6, and IL-1β in HUVECs. PARP1 was predicted and confirmed to be a target for albiflorin in vitro. Albiflorin targeted PARP1 to inhibit the activation of NF-κB. Transfection of HUVECs with PARP1 overexpression plasmids effectively reversed the effects of albiflorin on high glucose-treated HUVECs.

CONCLUSIONS

Albiflorin suppressed high glucose-induced endothelial cell apoptosis and inflammation, suggesting its potential in treating diabetic vascular complications. The action of albiflorin possibly caused by its regulation on inhibiting PARP1/NF-κB signaling.

摘要

目的

芍药长期以来被公认为一种具有抗炎作用的传统中药。我们旨在研究从芍药根中提取的活性成分芍药苷对糖尿病血管并发症的药理作用。

方法

用高糖刺激人脐静脉内皮细胞(HUVECs),并用5、10和20μM芍药苷进行处理。进行CCK-8检测、EdU染色、膜联蛋白V-FITC染色、Transwell检测、划痕试验、RT-PCR、ELISA、蛋白质印迹法和免疫荧光检测。使用SwissTargetPrediction数据库筛选芍药苷的靶点,并使用Autodock Vina软件进行分子对接。

结果

芍药苷处理可剂量依赖性减轻高糖诱导的HUVECs活力丧失。此外,芍药苷促进HUVECs的增殖和迁移,同时抑制其凋亡以及TNF-α、IL-6和IL-1β的释放。PARP1被预测并在体外证实为芍药苷的一个靶点。芍药苷靶向PARP1以抑制NF-κB的激活。用PARP1过表达质粒转染HUVECs可有效逆转芍药苷对高糖处理的HUVECs的作用。

结论

芍药苷抑制高糖诱导的内皮细胞凋亡和炎症,提示其在治疗糖尿病血管并发症方面的潜力。芍药苷的作用可能是通过其对PARP1/NF-κB信号通路的抑制调节所致。

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