ArticleDiabetes2008
Sulfasalazine blocks the development of tactile allodynia in diabetic rats.
Article in Diabetes, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 34 citations in OpenAlex.
- Peripheralized sepiapterin reductase inhibition as a safe analgesic therapy.Frontiers in pharmacology · 2023Review
- The Development of Mechanical Allodynia in Diabetic Rats Revealed by Single-Cell RNA-Seq.Frontiers in molecular neuroscience · 2022Article
- Loss of POMC-mediated antinociception contributes to painful diabetic neuropathy.Nature communications · 2021Article
- Prevalence of Migraine and Neuropathic Pain in Rheumatic Diseases.Journal of clinical medicine · 2020Article
- Antihyperalgesic Activity of Atomoxetine on Diabetes-Induced Neuropathic Pain: Contribution of Noradrenergic and Dopaminergic Systems.Molecules (Basel, Switzerland) · 2018Article
- Combining Human and Rodent Genetics to Identify New Analgesics.Neuroscience bulletin · 2018Review
- The effects of capillary dysfunction on oxygen and glucose extraction in diabetic neuropathy.Diabetologia · 2015Review
- Ciliary neurotrophic factor activates NF-κB to enhance mitochondrial bioenergetics and prevent neuropathy in sensory neurons of streptozotocin-induced diabetic rodents.Neuropharmacology · 2013Article
- Marrow-derived cells regulate the development of early diabetic retinopathy and tactile allodynia in mice.Diabetes · 2012Article
- Analgesia by inhibiting tetrahydrobiopterin synthesis.Current opinion in pharmacology · 2012Review
- A yeast-based screen reveals that sulfasalazine inhibits tetrahydrobiopterin biosynthesis.Nature chemical biology · 2011Article
- Article
- Review
- NF-κB subunits are differentially distributed in cells of lumbar dorsal root ganglia in naïve and diabetic rats.Neuroscience letters · 2011Article
- Beneficial effects of a novel RAGE inhibitor on early diabetic retinopathy and tactile allodynia.Molecular vision · 2011Article
- Comparison of three strains of diabetic rats with respect to the rate at which retinopathy and tactile allodynia develop.Molecular vision · 2010Article
- Effects of p38 MAPK inhibition on early stages of diabetic retinopathy and sensory nerve function.Investigative ophthalmology & visual science · 2010Article
- Diabetic painful and insensate neuropathy: pathogenesis and potential treatments.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2009Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveDiabetic neuropathy is manifested either by loss of nociception (painless syndrome) or by mechanical hyperalgesia and tactile allodynia (pain in response to nonpainful stimuli). While therapies with vasodilators or neurotrophins reverse some functional and metabolic abnormalities in diabetic nerves, they only partially ameliorate neuropathic pain. The reported link between nociception and targets of the anti-inflammatory drug sulfasalazine prompted us to investigate its effect on neuropathic pain in diabetes. RESEARCH DESIGN AND
methodsWe examined the effects of sulfasalazine, salicylates, and the poly(ADP-ribose) polymerase-1 inhibitor PJ34 on altered nociception in streptozotocin-induced diabetic rats. We also evaluated the levels of sulfasalazine targets in sciatic nerves and dorsal root ganglia (DRG) of treated animals. Finally, we analyzed the development of tactile allodynia in diabetic mice lacking expression of the sulfasalazine target nuclear factor-kappaB (NF-kappaB) p50.
resultsSulfasalazine completely blocked the development of tactile allodynia in diabetic rats, whereas relatively minor effects were observed with other salicylates and PJ34. Along with the behavioral findings, sciatic nerves and DRG from sulfasalazine-treated diabetic rats displayed a decrease in NF-kappaB p50 expression compared with untreated diabetic animals. Importantly, the absence of tactile allodynia in diabetic NF-kappaB p50(-/-) mice supported a role for NF-kappaB in diabetic neuropathy. Sulfasalazine treatment also increased inosine levels in sciatic nerves of diabetic rats.
conclusionsThe complete inhibition of tactile allodynia in experimental diabetes by sulfasalazine may stem from its ability to regulate both NF-kappaB and inosine. Sulfasalazine might be useful in the treatment of nociceptive alterations in diabetic patients.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.