Kageyama Yasunori, Takahashi Masaaki, Nagafusa Tetsuyuki, Torikai Eiji, Nagano Akira
Department of Orthopaedic Surgery, Hamamatsu University School of Medicine, 1-20-1 Handayama, Hamamatsu, 431-3125, Japan.
Mod Rheumatol. 2007;17(5):398-402. doi: 10.1007/s10165-007-0607-6. Epub 2007 Oct 19.
This study was performed to investigate whether methotrexate (MTX) affects the levels of oxidative stress markers, including pentosidine one of the glycation end products (AGEs) or 8-hydroxy-deoxy guanosine (8-OHdG). These stress markers represent DNA damage; 19 rheumatoid arthritis (RA) patients underwent MTX treatment. The levels of serum total, urinary total, urinary-free pentosidine and also urinary 8-OHdG, as well as clinical parameters, including disease activity scores for 28 joints (DAS28) were measured at baseline and at 3 and 6 months after the initial treatment with MTX. After the initial treatment with MTX, serum total and urinary total pentosidine levels were reduced at 6 months, and urinary-free pentosidine levels were reduced at 3 and 6 months. Urinary 8-OHdG levels also were significantly reduced at 6 months after the initial treatment with MTX. This study demonstrated that MTX plays a role as a regulator against pentosidine formation and oxidative DNA damage in RA patients.
本研究旨在调查甲氨蝶呤(MTX)是否会影响氧化应激标志物的水平,包括糖基化终产物(AGEs)之一的戊糖苷或8-羟基脱氧鸟苷(8-OHdG)。这些应激标志物代表DNA损伤;19名类风湿性关节炎(RA)患者接受了MTX治疗。在基线以及MTX初始治疗后的3个月和6个月,测量血清总戊糖苷、尿总戊糖苷、尿游离戊糖苷以及尿8-OHdG的水平,以及包括28个关节疾病活动评分(DAS28)在内的临床参数。MTX初始治疗后,血清总戊糖苷和尿总戊糖苷水平在6个月时降低,尿游离戊糖苷水平在3个月和6个月时降低。MTX初始治疗后6个月,尿8-OHdG水平也显著降低。本研究表明,MTX在RA患者中作为戊糖苷形成和氧化性DNA损伤的调节剂发挥作用。