关键词: Angelica Sinensis polysaccharide Bone modeling Gut microbiota Rheumatoid arthritis Tight junction Angelica Sinensis polysaccharide Bone modeling Gut microbiota Rheumatoid arthritis Tight junction

Mesh : Angelica sinensis / chemistry metabolism Animals Arthritis, Rheumatoid / drug therapy genetics metabolism Claudin-5 / biosynthesis genetics Gastrointestinal Microbiome Intestines / metabolism microbiology Membrane Proteins / biosynthesis genetics Polysaccharides / pharmacology RGS Proteins / biosynthesis genetics Rats Angelica sinensis / chemistry metabolism Animals Arthritis, Rheumatoid / drug therapy genetics metabolism Claudin-5 / biosynthesis genetics Gastrointestinal Microbiome Intestines / metabolism microbiology Membrane Proteins / biosynthesis genetics Polysaccharides / pharmacology RGS Proteins / biosynthesis genetics Rats

来  源:   DOI:10.1016/j.ijbiomac.2022.03.090

Abstract:
Rheumatoid arthritis (RA) is an autoimmune disease with a high incidence. Recent studies have demonstrated that diet can contribute to the development and progression of RA. Indeed, non-starch polysaccharides (NSPs) were known to be related to the improvement of RA. In this study, the collagen-induced rats were administrated with Angelica sinensis polysaccharide (ASP) at 200 mg/kg (L), 400 mg/kg (M), or 800 mg/kg (H). Results showed that ASP could reduce joint swelling and significantly inhibit anti-CII-antibodies and pro-inflammatory factors in RA, H group showed the best treatment among them. Further analysis using 16S rDNA sequencing suggested that ASP could shape the gut microbiota composition. Several key bacteria, including norank_f__norank_o__Clostridia_UCG-014, Lactobacillus, norank_f__Oscillospiraceae, and norank_f__Desulfovibrionaceae, were found to be related to the development of RA. The colonic transcriptome showed that ASP could restore RA-induced intestinal dysfunction, such as tight junction disarrangement, by upregulating Cldn5. The balance between osteoblasts and osteoclasts might be modified by regulating the expression of Slit3 and Rgs18 to alleviate RA, which may be correlated with gut microbiota. Our results suggested that ASP improved RA by regulating gut microbiota and gene expression, revealing a positive relationship between dietary patterns and RA.
摘要:
类风湿性关节炎(RA)是一种发病率较高的自身免疫性疾病。最近的研究表明,饮食可以促进RA的发生和发展。的确,已知非淀粉多糖(NSPs)与RA的改善有关。在这项研究中,胶原诱导大鼠服用当归多糖(ASP)200mg/kg(L),400mg/kg(M),或800mg/kg(H)。结果表明,ASP可以减轻RA的关节肿胀,并显着抑制抗CII抗体和促炎因子。其中H组治疗效果最好。使用16SrDNA测序的进一步分析表明,ASP可以塑造肠道微生物群组成。几种关键细菌,包括norank_f_norank_o__梭菌_UCG-014,乳酸杆菌,norank_f__蛇形科,和norank_f__脱硫弧菌科,被发现与RA的发展有关。结肠转录组显示ASP可以恢复RA引起的肠功能障碍,如紧密连接的排列,通过上调Cldn5。通过调节Slit3和Rgs18的表达来改善成骨细胞和破骨细胞之间的平衡,从而减轻RA的作用。这可能与肠道微生物群有关。我们的结果表明,ASP通过调节肠道菌群和基因表达来改善RA,揭示了膳食模式与RA之间的正相关关系。
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