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吡啶酮类糖基化终产物抑制剂减轻 2 型糖尿病大鼠椎间盘退变。

Advanced Glycation End Product Inhibitor Pyridoxamine Attenuates IVD Degeneration in Type 2 Diabetic Rats.

机构信息

Orthopaedic Stem Cell Research Laboratory, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.

Board of Governors Regenerative Medicine Institute, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.

出版信息

Int J Mol Sci. 2020 Dec 19;21(24):9709. doi: 10.3390/ijms21249709.

DOI:10.3390/ijms21249709
PMID:33352698
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7766438/
Abstract

Type 2 diabetes mellitus (T2DM) is associated with advanced glycation end product (AGE) enrichment and considered a risk factor for intervertebral disc (IVD) degeneration. We hypothesized that systemic AGE inhibition, achieved using pyridoxamine (PM), attenuates IVD degeneration in T2DM rats. To induce IVD degeneration, lumbar disc injury or sham surgery was performed on Zucker Diabetic Sprague Dawley (ZDSD) or control Sprague Dawley (SD) rats. Post-surgery, IVD-injured ZDSD rats received daily PM dissolved in drinking water or water only. The resulting groups were SD uninjured, SD injured, ZDSD uninjured, ZDSD injured, and ZDSD injured + PM. Levels of blood glycation and disc degeneration were investigated. At week 8 post-surgery, glycated serum protein (GSP) levels were increased in ZDSDs compared to SDs. PM treatment attenuated this increase. Micro-MRI analysis demonstrated IVD dehydration in injured versus uninjured SDs and ZDSDs. In the ZDSD injured + PM group, IVD dehydration was diminished compared to ZDSD injured. AGE levels were decreased and aggrecan levels increased in ZDSD injured + PM versus ZDSD injured rats. Histological and immunohistochemical analyses further supported the beneficial effect of PM. In summary, PM attenuated GSP levels and IVD degeneration processes in ZDSD rats, demonstrating its potential to attenuate IVD degeneration in addition to managing glycemia in T2DM.

摘要

2 型糖尿病（T2DM）与晚期糖基化终产物（AGE）的富集有关，被认为是椎间盘（IVD）退变的危险因素。我们假设使用吡哆胺（PM）进行系统性 AGE 抑制可以减轻 T2DM 大鼠的 IVD 退变。为了诱导 IVD 退变，对 Zucker 糖尿病 Sprague Dawley（ZDSD）或对照 Sprague Dawley（SD）大鼠进行腰椎间盘损伤或假手术。手术后，IVD 损伤的 ZDSD 大鼠每天接受溶于饮用水或仅水的 PM 治疗。得到的组为 SD 未损伤、SD 损伤、ZDSD 未损伤、ZDSD 损伤和 ZDSD 损伤+PM。研究了血液糖化和椎间盘退变的水平。手术后 8 周，与 SD 大鼠相比，ZDSD 大鼠的糖化血清蛋白（GSP）水平升高。PM 治疗减轻了这种增加。微 MRI 分析表明，与未损伤的 SD 和 ZDSD 相比，损伤的 IVD 脱水。在 ZDSD 损伤+PM 组中，与 ZDSD 损伤组相比，IVD 脱水减少。与 ZDSD 损伤组相比，ZDSD 损伤+PM 组的 AGE 水平降低，聚集蛋白水平升高。组织学和免疫组织化学分析进一步支持了 PM 的有益作用。总之，PM 减轻了 ZDSD 大鼠的 GSP 水平和 IVD 退变过程，表明其除了控制 T2DM 中的血糖外，还具有减轻 IVD 退变的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f09f/7766438/d98533581b62/ijms-21-09709-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f09f/7766438/d403804e81cf/ijms-21-09709-g001.jpg
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