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用抗CD20抗体利妥昔单抗治疗的类风湿性关节炎DBA/IJ小鼠模型中的非整倍体和染色体断裂改变。

Aneugenic and clastogenic alterations in the DBA/IJ mouse model of rheumatoid arthritis treated with rituximab, an anti-CD20 antibody.

作者信息

Attia Sabry M, Al-Hamamah Mohammed A, Alotaibi Moureq R, Alasmari Abdullah F, Attia Mohamed S M, Ahmad Sheikh F, Mahmoud Mohamed A, Nadeem Ahmed, Ansari Mushtaq A, Bakheet Saleh A

机构信息

Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia.

Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia.

出版信息

Mutat Res Genet Toxicol Environ Mutagen. 2023 May-Jun;888:503635. doi: 10.1016/j.mrgentox.2023.503635. Epub 2023 Apr 3.

DOI:10.1016/j.mrgentox.2023.503635
PMID:37188433
Abstract

Rheumatoid arthritis (RA), an autoimmune disorder in which the immune system attacks healthy cells, is associated with elevated risk of lymphoma. Rituximab, a treatment for non-Hodgkin's lymphoma, has been approved as a treatment for RA. We studied the effects of rituximab on chromosomal stability in collagen-induced arthritis DBA/1J animal models. Micronucleus levels were increased in the mouse models, mainly due to chromosome loss, as detected by fluorescence in situ hybridization; rituximab-treated arthritic mice had significantly less micronucleus formation. Serum 8-hydroxydeoxyguanosine, a DNA oxidative stress marker, was increased in the mice models but reduced following rituximab administration.

摘要

类风湿性关节炎(RA)是一种自身免疫性疾病,免疫系统会攻击健康细胞,它与淋巴瘤风险升高有关。利妥昔单抗是一种治疗非霍奇金淋巴瘤的药物,已被批准用于治疗RA。我们研究了利妥昔单抗对胶原诱导性关节炎DBA/1J动物模型染色体稳定性的影响。通过荧光原位杂交检测发现,小鼠模型中的微核水平升高,主要是由于染色体丢失;用利妥昔单抗治疗的关节炎小鼠微核形成明显减少。血清8-羟基脱氧鸟苷是一种DNA氧化应激标志物,在小鼠模型中升高,但在给予利妥昔单抗后降低。

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