ArticleJournal of diabetes and metabolic disorders2021
Benfotiamine reduced collagen IV contents of sciatic nerve in hyperglycemic rats.
Article in Journal of diabetes and metabolic disorders, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 7 citations in OpenAlex.
- Potential of Benfotiamine in the treatment of neuropsychological disorders.Molecular biology reports · 2025Review
- Effect of Hesperidin on Sciatic Nerve Damage in STZ-Induced Diabetic Neuropathy: Modulation of TRPM2 Channel.Neurotoxicity research · 2023Article
- Proteomic analysis of peripheral nerve myelin during murine aging.Frontiers in cellular neuroscience · 2023Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNeuropathy as a common complication of hyperglycemia in diabetic patients is probably caused by metabolic and structural changes in extracellular matrix (ECM) of peripheral nerves. This study was designed to evaluate the effects of benfotiamine (BT) on the structural, biological and mechanical characteristics of rat sciatic nerve in hyperglycemic condition. MATERIALS AND
methodsForty eight adult male Wistar rats were assigned to 6 groups (n = 8): control (healthy rats with no treatment; C), positive control (healthy rats received BT treatment; B), negative control groups 1&2 (hyperglycemic rats kept for 4 and/or 8 weeks; 4WD and 8WD, respectively) and experimental groups 1&2 (hyperglycemic rats treated by daily oral gavage of 100 mg kg
resultsIn comparison to control groups, in 4WD and 8WD groups the amount of type IV collagen was increased, the structure of myelin sheath and nerve fibers were extensively altered and the tensile strength was significantly decreased (
conclusionsIt seems that BT treatment may rescue the sciatic nerve from the hyperglycemic-induced ECM structural abnormality. This beneficial advantage of BT is likely exerted through the modification of glucose metabolism pathways.
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