Intake excessive arsenic (As) is related to the occurrence of peripheral neuropathy. However, both the underlying mechanism and the preventive approach remain largely unknown. In the present study, As treatment significantly decreased the mechanical withdrawal threshold and increased the titer of anti‐myelin basic protein antibody in rats, accompanied with damaged BNB. The levels of inflammatory cytokines and proteolytic enzymes were also significantly upregulated. However, administration of MeCbl in As‐treated rats significantly reversed the decline in hindfoot mechanical withdrawal threshold, as well as BNB failure and sciatic nerve inflammation. Repeated As treatment in athymic nude mice indicated that sciatic nerve inflammation and mechanical hyperalgesia were T cell‐dependent. These data implicated that MBP‐activated autoimmunity and the related neuroinflammation probably contributed to As‐induced mechanical hyperalgesia and MeCbl exerted a protective role probably via maintenance the integrity of BNB and inhibition of neuroinflammation.

中文翻译：

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MBP激活的自身免疫在砷引起的周围神经病变和甲钴胺的潜在保护作用中起作用

摄入过量的砷与周围神经病变的发生有关。然而，其基本机制和预防方法仍然很大程度上未知。在本研究中，As治疗显着降低了大鼠的机械退缩阈值并提高了抗髓磷脂碱性蛋白抗体的滴度，并伴有BNB受损。炎性细胞因子和蛋白水解酶的水平也显着上调。但是，在接受As治疗的大鼠中施用MeCbl可以显着逆转后足机械退缩阈值的下降，以及BNB衰竭和坐骨神经发炎。在无胸腺裸鼠中重复进行As治疗表明，坐骨神经发炎和机械性痛觉过敏是T细胞依赖性的。