ArticleMolecular medicine reports2017
The Toll-like receptor 4 antagonist TAK-242 protects against chronic pancreatitis in rats.
Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
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Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.
- Putative molecular targets for vitamin A in neutralizing oxidative stress in acute and chronic pancreatitis - a systematic review.Naunyn-Schmiedeberg's archives of pharmacology · 2023Pooled it
- Taking its TOLL: the role of toll-like receptor 4 in human health and disease, and its potential as a therapeutic target.Frontiers in immunology · 2026Review
- Novel Analgesics with Peripheral Targets.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2020Review
- Cystitis-induced bladder pain is Toll-like receptor 4 dependent in a transgenic autoimmune cystitis murine model: a MAPP Research Network animal study.American journal of physiology. Renal physiology · 2019Article
- Angiotensin 1-7 ameliorates caerulein-induced inflammation in pancreatic acinar cells by downregulating Toll-like receptor 4/nuclear factor-κB expression.Molecular medicine reports · 2018Article
- Augmenter of liver regeneration (ALR) regulates acute pancreatitis via inhibiting HMGB1/TLR4/NF-κB signaling pathway.American journal of translational research · 2018Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic pancreatitis is a progressive disease characterized by irreversible morphological changes to the pancreas, typically causing pain and permanent loss of function. It is a poorly understood disease with the pathogenesis remaining unclear. The authors' previous data demonstrated that the inhibition of Toll‑like receptor 4 (TLR4) using TLR4 antagonist kinase (TAK)‑242 attenuates taurocholate‑induced oxidative stress via the regulation of mitochondrial function in the pancreatic acinar cells of mice. In the present study, the effect of TAK‑242 on trinitrobenzene sulfonic acid (TNBS)‑induced chronic pancreatitis was investigated in rats. The results revealed that TAK‑242 attenuated the severity of chronic pancreatic injury, and regulated extracellular matrix secretion and cellular immunity. In addition, TAK‑242 treatment significantly decreased cell apoptosis, as evidenced by the reduction in Terminal deoxynucleotidyl transferase dUTP nick end labeling‑positive cells in pancreas tissue sections, and also promoted cell proliferation in TNBS‑treated animals. Furthermore, the results of the calibrated von Frey filament assay demonstrated that TAK‑242 could prevent the pancreatitis‑induced referred abdominal hypersensitivity. In summary, TAK‑242 exhibits protective effects against TNBS‑induced chronic pancreatitis and may be a potential therapeutic strategy for the treatment of patients with chronic pancreatitis.
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Registered trials
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