Benfotiamine relieves inflammatory and neuropathic pain in rats

Sánchez-Ramírez, Gabriela M.; Caram-Salas, Nadia L.; Rocha-González, Héctor Isaac; Vidal‐Cantú, Guadalupe C.; Medina-Santillán, Roberto; Reyes-Garcı́a, Gerardo; Granados‐Soto, Vinicio

doi:10.1016/j.ejphar.2005.11.016

Cited by 71 publications

(43 citation statements)

References 29 publications

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“…BF has been shown to reduce diabetes-induced tissue damage in vivo and in vitro. 6,[22][23][24][25][26][27][28][29] Until now there have been no data available dealing with uremia or PD. We chose to use BF rather than thiamine for these studies because it has a higher bioavailability than thiamine.…”

Section: Discussionmentioning

confidence: 99%

Benfotiamine Protects against Peritoneal and Kidney Damage in Peritoneal Dialysis

Kihm

Müller-Krebs

Klein

et al. 2011

Journal of the American Society of Nephrology

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Section: Discussionmentioning

confidence: 99%

Benfotiamine Protects against Peritoneal and Kidney Damage in Peritoneal Dialysis

Kihm

Müller-Krebs

Klein

et al. 2011

Journal of the American Society of Nephrology

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“…In addition, it has shown beneficial acute and chronic anti-inflammatory actions upon induced skin lesions (49). Further studies in diabetic neuropathy have shown a beneficial effect of benfotiamine upon several modalities of neuropathic pain (50) and another study in humans suggested benfotiamine improved pain in diabetic polyneuropathy (51).…”

Section: Thiamine and Vascular Diseasementioning

confidence: 99%

Thiamine deficiency in diabetes mellitus and the impact of thiamine replacement on glucose metabolism and vascular disease

Page

Laight

Cummings

2011

International Journal of Clinical Practice

115

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Summary Despite the targeting of traditional risk factors for cardiovascular disease, disease burden has not been completely eliminated. Thiamine is an essential cofactor in carbohydrate metabolism and individuals with diabetes are thiamine deficient. The pathophysiology of recognised complications of thiamine deficiency is similar to that underlying atherosclerosis and the metabolic syndrome, namely oxidative stress, inflammation and endothelial dysfunction. This review examines the mechanisms by which thiamine deficiency occurs in individuals with diabetes, how this deficiency leads to hyperglycaemic‐induced damage, and the effect of thiamine replacement on vascular disease, endothelial function and oxidative stress. Thiamine administration can prevent the formation of harmful by‐products of glucose metabolism, reduce oxidative stress and improve endothelial function. The potential benefit of long‐term replacement in those with diabetes is not yet known but may reduce cardiovascular risk and angiopathic complications.

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“…The latter is consistent with less severe or absent tactile allodynia in STZ-diabetic inducible nitric oxide synthasedeficient and PARP-deficient mice, compared with the corresponding wild-type mice with STZ-diabetes of similar severity and duration. 14,44 Other agents effective against tactile allodynia in STZ-diabetic rat model include nitecapone, a catechol-O-methyltransferase inhibitor with potent antioxidant properties, 91 agmatine, an endogenous cationic amine resulting from the decarboxylation of L-arginine, 92 allopurinol, 28 interleukin-6, 31 melatonin, 93 benfotiamine, 94 and the cannabinoid agonist WIN 55,212-2, 95 as well as a cocktail of B 1 , B 6 , and B 12 vitamins. 96 Tactile allodynia in STZ-diabetic mice was found preventable by sulfasalazine, probably via blockage of NF-B activation, 87 as well as the cyclooxygenase-2 inhibitor meloxicam 97 and the 12/15-lipoxygenase inhibitors baicalein and cinnamyl-3,4-dihydroxy-␣-cyanocinnamate.…”

Section: Diabetes-associated Tactile Allodyniamentioning

confidence: 99%

Diabetic Painful and Insensate Neuropathy: Pathogenesis and Potential Treatments

2009

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Summary:Advanced peripheral diabetic neuropathy (PDN) is associated with elevated vibration and thermal perception thresholds that progress to sensory loss and degeneration of all fiber types in peripheral nerve. A considerable proportion of diabetic patients also describe abnormal sensations such as paresthesias, allodynia, hyperalgesia, and spontaneous pain. One or several manifestations of abnormal sensation and pain are described in all the diabetic rat and mouse models studied so far (i.e., streptozotocin-diabetic rats and mice, type 1 insulinopenic BB/Wor and type 2 hyperinsulinemic diabetic BBZDR/Wor rats, Zucker diabetic fatty rats, and nonobese diabetic, Akita, leptin-and leptin-receptor-deficient, and highfat diet-fed mice). Such manifestations are 1) thermal hyperalgesia, an equivalent of a clinical phenomenon described in early PDN; 2) thermal hypoalgesia, typically present in advanced PDN; 3) mechanical hyperalgesia, an equivalent of pain on pressure in early PDN; 4) mechanical hypoalgesia, an equivalent to the loss of sensitivity to mechanical noxious stimuli in advanced PDN; 5) tactile allodynia, a painful perception of a light touch; and 5) formalin-induced hyperalgesia. Rats with short-term diabetes develop painful neuropathy, whereas those with longer-term diabetes and diabetic mice typically display manifestations of both painful and insensate neuropathy, or insensate neuropathy only. Animal studies using pharmacological and genetic approaches revealed important roles of increased aldose reductase, protein kinase C, and poly(ADPribose) polymerase activities, advanced glycation end-products and their receptors, oxidative-nitrosative stress, growth factor imbalances, and C-peptide deficiency in both painful and insensate neuropathy. This review describes recent achievements in studying the pathogenesis of diabetic neuropathic pain and sensory disorders in diabetic animal models and developing potential pathogenetic treatments. Key Words: Animal models, diabetic insensate neuropathy, diabetic painful neuropathy, formalin-induced hyperalgesia, mechanical hyper-and hypoalgesia, pathogenetic treatments of diabetic neuropathic pain and sensory loss, symptomatic treatments of diabetic pain, tactile allodynia, thermal hyper-and hypoalgesia.

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Benfotiamine relieves inflammatory and neuropathic pain in rats

Cited by 71 publications

References 29 publications

Benfotiamine Protects against Peritoneal and Kidney Damage in Peritoneal Dialysis

Benfotiamine Protects against Peritoneal and Kidney Damage in Peritoneal Dialysis

Thiamine deficiency in diabetes mellitus and the impact of thiamine replacement on glucose metabolism and vascular disease

Diabetic Painful and Insensate Neuropathy: Pathogenesis and Potential Treatments

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