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首页> 外文期刊>Life sciences >Pentadecapeptide BPC 157 and its effects on a NSAID toxicity model: diclofenac-induced gastrointestinal, liver, and encephalopathy lesions.
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Pentadecapeptide BPC 157 and its effects on a NSAID toxicity model: diclofenac-induced gastrointestinal, liver, and encephalopathy lesions.

机译：五肽肽BPC 157及其对NSAID毒性模型的影响：双氯芬酸诱导的胃肠道，肝脏和脑病病变。

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AIMS: We attempted to fully antagonize the extensive toxicity caused by NSAIDs (using diclofenac as a prototype). MAIN METHODS: 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. KEY FINDINGS: Already considered a drug that can reverse the toxic side effects of NSAIDs, BPC 157 (10 mug/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 mug/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). SIGNIFICANCE: The very extensive antagonization of diclofenac toxicity achieved with BPC 157 (mug-g-regimen, intraperitoneally, per-orally) may encourage its further use as a therapy to counteract diclofenac- and other NSAID-induced toxicity.
机译：目的：我们试图完全对抗由非甾体抗炎药引起的广泛毒性（使用双氯芬酸作为原型）。主要方法：本文中，我们使用稳定的胃五肽BPC 157（GEPPPGKPADDAGLV，MW 1419），一种抗溃疡肽，在炎症性肠病临床试验（PL 14736）和各种伤口治疗中均显示出有效的作用，但未见毒性报告。给予该肽拮抗双氯芬酸（12.5mg / kg腹膜内，每天一次，连续3天）诱导的胃肠道，肝脏和脑的联合毒性。主要发现：已经考虑过可以逆转NSAIDs毒性副作用的药物，在（i）双氯芬酸治疗后立即腹膜内给予（i）BPC 157（10杯/千克，10 ng / kg）在整个实验中都非常有效。口服（0.16杯/毫升，0.16纳克/毫升）。如果没有BPC 157治疗，在最后一次双氯芬酸攻击后3小时，我们会遇到双氯芬酸毒性的复杂有害循环，其特征是严重的胃，肠和肝损伤，胆红素升高，天冬氨酸转氨酶（AST），丙氨酸转氨酶（ALT）血清值升高肝脏重量，长时间的镇静/神志不清（任何双氯芬酸攻击后），最后是肝性脑病（脑水肿，特别是位于大脑皮层和小脑，白色而不是灰质），红色神经元受损，尤其是在大脑皮层和小脑核中，浦肯野细胞和海马神经元中较少见。意义：用BPC 157（杯子/ ng方案，腹膜内，口服）对双氯芬酸的毒性有非常广泛的拮抗作用，这可能鼓励其进一步用作对抗双氯芬酸和其他NSAID诱导的毒性的疗法。

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