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异钩藤碱通过 NF-κB/NLRP3 信号通路抑制内皮细胞和巨噬细胞的炎症反应。

Isorhynchophylline inhibits inflammatory responses in endothelial cells and macrophages through the NF-κB/NLRP3 signaling pathway.

机构信息

Innovative Institute of Chinese Medicine and Pharmacy, Shandong University of Traditional Chinese Medicine, Jinan, 250000, China.

Shandong University of Traditional Chinese Medicine, Jinan, 250000, China.

出版信息

BMC Complement Med Ther. 2023 Mar 11;23(1):80. doi: 10.1186/s12906-023-03902-3.

DOI:10.1186/s12906-023-03902-3
PMID:36906555
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10007741/
Abstract

BACKGROUND

Atherosclerosis is a chronic inflammatory disease of arterial wall, which is closely related to inflammatory reaction. In this study, the anti-inflammatory effect of isorhynchophylline was studied by NF- κB / NLRP3 pathway.

METHODS

(1) ApoE mice were fed with high-fat diet to establish atherosclerotic model, while C57 with the same genetic background was fed with common diet as control group. Body weight was recorded and blood lipids were detected. The expression of NLRP3, NF-κB, IL-18 and Caspase-1 in aorta was detected by Western-Blot and PCR, and plaque formation was detected by HE and oil red O staining. (2) Lipopolysaccharide interfered with Human Umbilical Vein Endothelial Cells (HUVECs) and RAW264.7 to form inflammatory model, and was treated with isorhynchophylline. The expression of NLRP3, NF-κB, IL-18 and Caspase-1 in aorta was detected by Western-Blot and PCR, and the ability of cell migration was detected by Transwell and scratch test.

RESULTS

(1) the expression of NLRP3, NF- κB, IL-18 and Caspase-1 in aorta of model group was higher than that of control group, and plaque formation was obvious. (2) the expressions of NLRP3, NF- κB, IL-18 and Caspase-1 in HUVECs and RAW264.7 model groups were higher than those in control group, while isorhynchophylline decreased their expression and enhanced cell migration ability.

CONCLUSION

Isorhynchophylline can reduce the inflammatory reaction induced by lipopolysaccharide and promote the ability of cell migration.

摘要

背景

动脉粥样硬化是动脉壁的一种慢性炎症性疾病,与炎症反应密切相关。本研究通过 NF-κB/NLRP3 通路研究了异钩藤碱的抗炎作用。

方法

(1)用高脂饮食喂养 ApoE 小鼠建立动脉粥样硬化模型,同时用相同遗传背景的 C57 作为对照组用普通饮食喂养。记录体重,检测血脂。通过 Western-Blot 和 PCR 检测主动脉中 NLRP3、NF-κB、IL-18 和 Caspase-1 的表达,并通过 HE 和油红 O 染色检测斑块形成。(2)用脂多糖干扰人脐静脉内皮细胞(HUVECs)和 RAW264.7 形成炎症模型,并用异钩藤碱处理。通过 Western-Blot 和 PCR 检测主动脉中 NLRP3、NF-κB、IL-18 和 Caspase-1 的表达,并通过 Transwell 和划痕试验检测细胞迁移能力。

结果

(1)模型组主动脉中 NLRP3、NF-κB、IL-18 和 Caspase-1 的表达高于对照组,斑块形成明显。(2)HUVECs 和 RAW264.7 模型组中 NLRP3、NF-κB、IL-18 和 Caspase-1 的表达高于对照组,而异钩藤碱降低了它们的表达并增强了细胞迁移能力。

结论

异钩藤碱可减轻脂多糖诱导的炎症反应,促进细胞迁移能力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34c5/10007741/ec133e95c164/12906_2023_3902_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34c5/10007741/82a5cca48cde/12906_2023_3902_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34c5/10007741/be98aa930272/12906_2023_3902_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34c5/10007741/03e944b9b23c/12906_2023_3902_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34c5/10007741/8f2e41c45b79/12906_2023_3902_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34c5/10007741/ec133e95c164/12906_2023_3902_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34c5/10007741/82a5cca48cde/12906_2023_3902_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34c5/10007741/be98aa930272/12906_2023_3902_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34c5/10007741/03e944b9b23c/12906_2023_3902_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34c5/10007741/8f2e41c45b79/12906_2023_3902_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34c5/10007741/ec133e95c164/12906_2023_3902_Fig5_HTML.jpg

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