Department of Rheumatology, First Affiliated Hospital of Anhui University of Traditional Chinese Medicine (TCM), Hefei, Anhui, China (mainland).
Med Sci Monit. 2019 Sep 9;25:6767-6774. doi: 10.12659/MSM.916317.
BACKGROUND Rheumatoid arthritis (RA) is a chronic autoimmune disease targeting joints. This research aimed to explore the effects of Xinfeng capsules (XFC) on cardiac injury in adjuvant arthritis (AA) model rats and assessed the associated mechanism. MATERIAL AND METHODS An adjuvant arthritis (AA) rat model was established by intracutaneously injection with Freund's complete adjuvant (FCA). Model rats were divided into 4 groups: an AA model group, an astragalus polysaccharides (APS) group, a methotrexate (MTX) group, and an XFC and triptolide (TPT) group. Hematoxylin-eosin (HE) staining was used to observe histopathologic changes. TUNEL assay was utilized to evaluate the apoptosis of cardiomyocytes. ELISA was utilized to evaluate levels of tumor necrosis factor alpha (TNF-alpha), interleukin 17 (IL-17), and interleukin 6 (IL-6) in myocardial tissues. Quantitative RT-PCR (qRT-PCR) was used to detect microRNA-21 (miRNA21) levels. Mitogen-activated protein kinase (MAPK)/p38, Toll-like receptor 4 (TLR4), and nuclear kappa B (NF-kappaB)/p65 levels were evaluated using Western blot. RESULTS XFC significantly improved proinflammatory response compared to the AA model group (p<0.05). XFC treatment significantly decreased the number of cells staining TUNEL-positive compared with the model group (p<0.05). XFC treatment significantly reduced TNF-alpha, IL-17, and IL-6 levels in myocardial tissues compared to the model group (p<0.05). Levels of miRNA21 were significantly lower in the XFC group compared to the AA model group (p<0.05). TLR4, MAPK/p38, and NF-kappaB/p65 expression levels were significantly lower in the XFC group than in the model group (p<0.05). CONCLUSIONS Xinfeng capsule, a traditional Chinese medicine preparation, protects against cardiac injury in AA rats by modulating proinflammatory cytokines expression via the TLR4/MAPK/NF-kappaB signaling pathway.
类风湿关节炎（RA）是一种针对关节的慢性自身免疫性疾病。本研究旨在探讨新风胶囊（XFC）对佐剂性关节炎（AA）模型大鼠心脏损伤的影响，并评估其相关机制。
通过皮内注射弗氏完全佐剂（FCA）建立佐剂性关节炎（AA）大鼠模型。将模型大鼠分为 4 组：AA 模型组、黄芪多糖（APS）组、甲氨蝶呤（MTX）组、XFC 和雷公藤内酯醇（TPT）组。苏木精-伊红（HE）染色观察组织病理学变化。TUNEL 法评估心肌细胞凋亡。ELISA 法检测心肌组织中肿瘤坏死因子-α（TNF-α）、白细胞介素 17（IL-17）和白细胞介素 6（IL-6）水平。定量 RT-PCR（qRT-PCR）检测 microRNA-21（miRNA21）水平。Western blot 法检测丝裂原活化蛋白激酶（MAPK）/p38、Toll 样受体 4（TLR4）和核因子-κB（NF-κB）/p65 水平。
与 AA 模型组相比，XFC 显著改善了促炎反应（p<0.05）。XFC 治疗组与模型组相比，TUNEL 阳性细胞数明显减少（p<0.05）。XFC 治疗组心肌组织 TNF-α、IL-17 和 IL-6 水平明显低于模型组（p<0.05）。XFC 组 miRNA21 水平明显低于 AA 模型组（p<0.05）。XFC 组 TLR4、MAPK/p38 和 NF-κB/p65 表达水平明显低于模型组（p<0.05）。
中药新风胶囊通过 TLR4/MAPK/NF-κB 信号通路调节促炎细胞因子的表达，对 AA 大鼠心脏损伤起保护作用。
