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SHR Neuro Cancer Cardio Lipid Metab Microb
Ilic, S; Drmic, D; Franjic, S; Kolenc, D; Coric, M; Brcic, L; Klicek, R; Radic, B; Sever, M; Djuzel, V; Filipovic, M; Djakovic, Z; Stambolija, V; Blagaic, AB; Zoricic, I; Gjurasin, M; Stupnisek, M; Romic, Z; Zarkovic, K; Dzidic, S; Seiwerth, S; Sikiric, P.
Pentadecapeptide BPC 157 and its effects on a NSAID toxicity model: diclofenac-induced gastrointestinal, liver, and encephalopathy lesions.
Life Sci. 2011; 88(11-12): 535-542.
Doi: 10.1016/j.lfs.2011.01.015
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PubMed
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- Brcic Luka
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- Abstract:
- We attempted to fully antagonize the extensive toxicity caused by NSAIDs (using diclofenac as a prototype). Herein, we used the stable gastric pentadecapeptide BPC 157 (GEPPPGKPADDAGLV, MW 1419), an anti-ulcer peptide shown to be efficient in inflammatory bowel disease clinical trials (PL 14736) and various wound treatments with no toxicity reported. This peptide was given to antagonize combined gastrointestinal, liver, and brain toxicity induced by diclofenac (12.5mg/kg intraperitoneally, once daily for 3 days) in rats. Already considered a drug that can reverse the toxic side effects of NSAIDs, BPC 157 (10 μg/kg, 10 ng/kg) was strongly effective throughout the entire experiment when given (i) intraperitoneally immediately after diclofenac or (ii) per-orally in drinking water (0.16 μg/mL, 0.16 ng/mL). Without BPC 157 treatment, at 3h following the last diclofenac challenge, we encountered a complex deleterious circuit of diclofenac toxicity characterized by severe gastric, intestinal and liver lesions, increased bilirubin, aspartate transaminase (AST), alanine transaminase (ALT) serum values, increased liver weight, prolonged sedation/unconsciousness (after any diclofenac challenge) and finally hepatic encephalopathy (brain edema particularly located in the cerebral cortex and cerebellum, more in white than in gray matter, damaged red neurons, particularly in the cerebral cortex and cerebellar nuclei, Purkinje cells and less commonly in the hippocampal neurons). The very extensive antagonization of diclofenac toxicity achieved with BPC 157 (μg-/ng-regimen, intraperitoneally, per-orally) may encourage its further use as a therapy to counteract diclofenac- and other NSAID-induced toxicity. Copyright © 2011 Elsevier Inc. All rights reserved.
- Find related publications in this database (using NLM MeSH Indexing)
- Administration, Oral -
- Animals -
- Anti-Inflammatory Agents, Non-Steroidal -
- Anti-Ulcer Agents - administration & dosage Anti-Ulcer Agents - therapeutic use
- Behavior, Animal - drug effects
- Diclofenac -
- Disease Models, Animal -
- Drug-Induced Liver Injury - etiology Drug-Induced Liver Injury - pathology Drug-Induced Liver Injury - prevention & control
- Gastric Mucosa - drug effects Gastric Mucosa - pathology
- Gastrointestinal Diseases - chemically induced Gastrointestinal Diseases - pathology Gastrointestinal Diseases - prevention & control
- Hepatic Encephalopathy - etiology Hepatic Encephalopathy - pathology Hepatic Encephalopathy - prevention & control
- Injections, Intraperitoneal -
- Intestinal Mucosa - drug effects Intestinal Mucosa - pathology
- Liver Function Tests -
- Male -
- Peptide Fragments - administration & dosage Peptide Fragments - therapeutic use
- Proteins - administration & dosage Proteins - therapeutic use
- Rats -
- Rats, Wistar -
- Find related publications in this database (Keywords)
- BPC 157
- Diclofenac
- NSAIDs
- Toxicity
- Rats