A platform for research: civil engineering, architecture and urbanism
A platform for research: civil engineering, architecture and urbanism
MBP‐activated autoimmunity plays a role in arsenic‐induced peripheral neuropathy and the potential protective effect of mecobalamin
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.
MBP‐activated autoimmunity plays a role in arsenic‐induced peripheral neuropathy and the potential protective effect of mecobalamin
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.
MBP‐activated autoimmunity plays a role in arsenic‐induced peripheral neuropathy and the potential protective effect of mecobalamin
He, Qican (author) / Chen, Bingzhi (author) / Chen, Shaoyi (author) / Zhang, Muyang (author) / Duan, Lidan (author) / Feng, Xiangling (author) / Chen, Jihua (author) / Zhou, Lezhou (author) / Chen, Lv (author) / Duan, Yanying (author)
Environmental Toxicology ; 36 ; 1243-1253
2021-06-01
11 pages
Article (Journal)
Electronic Resource
English
Protective role of Allicin on Arsenic Induced Haematological and Renal Toxicity
| Springer Verlag | 2025
Neuropathy in Arsenic Toxicity from Groundwater Arsenic Contamination in West Bengal, India
| Online Contents | 2003
Arsenic as protective agent for cement
Engineering Index Backfile | 1931
| Wiley | 2025