Reviews BPC 157 as a therapy for severe electrolyte disturbances in rats—specifically hyperkalemia, hypokalemia, hypermagnesemia, and lithium toxicity. In each model, BPC 157 counteracted life-threatening cardiovascular and neuromuscular complications including arrhythmias, paralysis, and lethal outcomes. Suggests BPC 157's cytoprotective mechanism applies broadly to electrolyte-induced organ dysfunction.
Abstract
This review explores the therapeutic potential of the stable gastric pentadecapeptide BPC 157 in addressing electrolyte imbalances, specifically hyperkalemia, hypokalemia, hypermagnesemia, and hyperlithiemia. In hyperkalemia, BPC 157 demonstrated a comprehensive counteractive effect against KCl overdose (intraperitoneally, intragastrically, and in vitro), effectively mitigating symptoms such as muscular weakness, hypertension, sphincter dysfunction, arrhythmias, and lethality. It also counteracted the adverse effects of succinylcholine and magnesium overdose, including systemic muscle paralysis, arrhythmias, and hyperkalemia. In hypokalemia, BPC 157 (administered prophylactically or therapeutically, intraperitoneally or intragastrically) prevented fatal outcomes and addressed furosemide-induced hypokalemia, ECG changes, AV conduction block, ventricular arrhythmias, and skeletal muscle myoclonus. Following magnesium overdose, BPC 157 alleviated muscle weakness, brain lesions, and hyperkalemiainduced complications. In vitro studies (HEK293 cells) revealed the ability of BPC 157 to counteract hyperkalemia- and hypermagnesemia-induced depolarization and hypokalemia-induced hyperpolarization. In lithium intoxication, BPC 157 promoted collateral pathway activation, resolved vascular and multiorgan failure, and counteracted advanced Virchow triad conditions and occlusion-like syndromes. Collectively, these findings underscore the therapeutic promise of BPC 157 in managing electrolyte imbalances and warrant further investigation.