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黄连素对佐剂诱导的大鼠类风湿性关节炎的抗关节炎作用。

Anti-arthritic effect of berberine on adjuvant-induced rheumatoid arthritis in rats.

作者信息

Wang Xue, He Xin, Zhang Chun-Feng, Guo Chang-Run, Wang Chong-Zhi, Yuan Chun-Su

机构信息

State Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing 210009, China.

School of Pharmacy, Queen's University of Belfast, Belfast BT7 1NN, Northern Ireland, UK.

出版信息

Biomed Pharmacother. 2017 May;89:887-893. doi: 10.1016/j.biopha.2017.02.099. Epub 2017 Mar 7.

Abstract

BACKGROUND

Rheumatoid arthritis (RA) is a chronic and systemic autoimmune disease, which affects approximately 1% adult population in the worldwide.

AIM

The present study was to investigate the anti-arthritic effect of berberine and its involved mechanism in Freund's complete adjuvant (FCA) induced arthritis rats.

METHODS AND MATERIALS

Rats were divided randomly into control, FCA, tripterysium glycosides, berberine (75 and 150mg/kg). The apparent indicators, including changes of body weights, paw swelling degrees and arthritis indexes, were analyzed to evaluate anti-arthritic effect of berberine. The levels of IL-6, IL-10, IL-17 and TGF-β in serum were measured by ELISA. Histopathological changes and immunohistochemical expression of anti-IL-10 and anti-IL-17 antibodies in ankle joint tissues were examined.

RESULTS

Berberine obviously suppressed the severity of RA rats by attenuating the apparent indicators as mentioned above. Meanwhile, berberine significantly decreased the levels of IL-6 and IL-17, and increased the levels of IL-10 and TGF-β. Histopathological examinations indicated that berberine attenuated the synovial hyperplasia and inflammatory cell infiltration in joint tissues. In addition, immunohistochemical results showed that the amount of anti-IL-10 antibody increased, while the amount of anti-IL-17 antibody decreased in ankle tissues of arthritis rats.

CONCLUSIONS

Our results showed that berberine exerted a superior anti-arthritic effect and the mechanism maybe involve the balance between Treg and Th17 cells.

摘要

背景

类风湿性关节炎(RA)是一种慢性全身性自身免疫性疾病,全球约1%的成年人受其影响。

目的

本研究旨在探讨小檗碱对弗氏完全佐剂(FCA)诱导的关节炎大鼠的抗关节炎作用及其作用机制。

方法和材料

将大鼠随机分为对照组、FCA组、雷公藤多苷组、小檗碱(75和150mg/kg)组。分析包括体重变化、 paw肿胀程度和关节炎指数在内的表观指标,以评估小檗碱的抗关节炎作用。通过ELISA检测血清中IL-6、IL-10、IL-17和TGF-β的水平。检查踝关节组织的组织病理学变化以及抗IL-10和抗IL-17抗体的免疫组化表达。

结果

小檗碱通过减轻上述表观指标明显抑制了RA大鼠的病情严重程度。同时,小檗碱显著降低了IL-6和IL-17的水平,并提高了IL-10和TGF-β的水平。组织病理学检查表明,小檗碱减轻了关节组织中的滑膜增生和炎性细胞浸润。此外,免疫组化结果显示,关节炎大鼠踝关节组织中抗IL-10抗体量增加,而抗IL-17抗体量减少。

结论

我们的结果表明,小檗碱具有优异的抗关节炎作用,其机制可能涉及调节性T细胞(Treg)和辅助性T细胞17(Th17)之间的平衡。

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