青藤碱通过抑制血管生成缓解胶原诱导性关节炎小鼠。
Sinomenine mitigates collagen-induced arthritis mice by inhibiting angiogenesis.
机构信息
Third-Grade Pharmacological Laboratory on Chinese Medicine Approved by State Administration of Traditional Chinese Medicine, Medical College of China Three Gorges University, Yichang, Hubei, 443002, China; Shenzhen Institute of Geriatrics, Shenzhen, Guangdong, 518020, China; The Institute of Rheumatology, The First College of Clinical Medical Sciences, China Three Gorges University, Yichang, Hubei, 443003, China.
Third-Grade Pharmacological Laboratory on Chinese Medicine Approved by State Administration of Traditional Chinese Medicine, Medical College of China Three Gorges University, Yichang, Hubei, 443002, China.
出版信息
Biomed Pharmacother. 2019 May;113:108759. doi: 10.1016/j.biopha.2019.108759. Epub 2019 Mar 8.
OBJECTIVE
The objective of the present study is to investigate the inhibitory effects of sinomenine (SIN) on angiogenesis in a collagen-induced arthritis (CIA) mouse model.
METHODS
Arthritis assessments for all mice were recorded. The histopathological assessments were performed following haematoxylin and eosin (HE) staining. Immunohistochemistry and enzyme-linked immunosorbent assay (ELISA) analyses were used to detect the expression of hypoxia-inducible factor-1α (HIF-1α), vascular endothelial growth factor (VEGF) and angiopoietin 1 (ANG-1) in the serum and in the membrane. Immunohistochemistry was employed to detect the synovium microvessel density (MVD).
RESULTS
Compared with the CIA model group, SIN significantly ameliorated swelling and erythema extension, decreased the arthritis index, reduced inflammation, cartilage damage and bone erosion, and lessened the number of CD31 positive cells on the synovium. Moreover, the levels of HIF-1α, VEGF and ANG-1 in the synovium and in the peripheral serum were increased in the untreated CIA model group but were significantly reduced in the 30 mg/kg, 100 mg/kg and 300 mg/kg SIN treatment groups.
CONCLUSION
SIN could mitigate CIA by inhibiting angiogenesis, and the mechanism may associate with the HIF-1α-VEGF-ANG-1 axis. Additionally, our study provides a referable experimental basis for the use of SIN for the treatment of rheumatoid arthritis.
目的
本研究旨在探讨青藤碱（SIN）对胶原诱导性关节炎（CIA）小鼠模型中血管生成的抑制作用。
方法
记录所有小鼠的关节炎评估情况。采用苏木精和伊红（HE）染色进行组织病理学评估。采用免疫组织化学和酶联免疫吸附试验（ELISA）分析检测血清和膜中缺氧诱导因子-1α（HIF-1α）、血管内皮生长因子（VEGF）和血管生成素 1（ANG-1）的表达。采用免疫组织化学检测滑膜微血管密度（MVD）。
结果
与 CIA 模型组相比，SIN 显著改善了肿胀和红斑扩展，降低了关节炎指数，减少了炎症、软骨损伤和骨侵蚀，减少了滑膜上 CD31 阳性细胞的数量。此外，未经治疗的 CIA 模型组滑膜和外周血清中的 HIF-1α、VEGF 和 ANG-1 水平升高，但在 30mg/kg、100mg/kg 和 300mg/kg SIN 治疗组中显著降低。
结论
SIN 可通过抑制血管生成来减轻 CIA，其机制可能与 HIF-1α-VEGF-ANG-1 轴有关。此外，本研究为 SIN 治疗类风湿关节炎提供了可参考的实验依据。
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