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MBP ‐activated autoimmunity plays a role in arsenic‐induced peripheral neuropathy and the potential protective effect of mecobalamin
Author(s) -
He Qican,
Chen Bingzhi,
Chen Shaoyi,
Zhang Muyang,
Duan Lidan,
Feng Xiangling,
Chen Jihua,
Zhou Lezhou,
Chen Lv,
Duan Yanying
Publication year - 2021
Publication title -
environmental toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.813
H-Index - 77
eISSN - 1522-7278
pISSN - 1520-4081
DOI - 10.1002/tox.23122
Subject(s) - neuroinflammation , sciatic nerve , inflammation , peripheral neuropathy , hyperalgesia , autoimmunity , arsenic poisoning , myelin , immunology , chemistry , pharmacology , endocrinology , medicine , arsenic , central nervous system , antibody , receptor , organic chemistry , nociception , diabetes mellitus
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.